Cardiomyocyte apoptosis infarct ischemia reperfusion. Medical search. Frequent questions

In mice knock down or inhibition of specific platelets proteins like PAR-4, GPVI or P-selectin leads to reduced infarct size and reduced inflammation in the acute phase after I/R injury. (isth.org)
Thrombocytopenia in mice leads to reduced infarct size and an improved left ventricular function 24 hours and 21 days after myocardial infarction. (isth.org)

The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
Neonatal rat cardiomyocytes were isolated and subjected to hypoxia/reoxygenation (H/R) injury, with or without HPC. (spandidos-publications.com)
However, in spite of their resistance to hypoxia only a small portion of cells survive when transplanted into an infarct scar (6). (escardio.org)
Ischemia/reperfusion (I/R) in mouse hearts and hypoxia/oxidative stress in neonatal rat cardiomyocytes have been associated with a downregulation of MG53. (biomedcentral.com)
Hypoxia/reoxygenation (H/R)-induced cardiomyocyte cell apoptosis is critical in developing myocardial infarction. (biomedcentral.com)
Rat cardiomyocyte H9c2 cells underwent H/R (hypoxia for 4 h and reoxygenation for 12 h). (biomedcentral.com)
Myocardial ischemia, also called cardiac ischemia or hypoxia/reoxygenation (H/R)-induced heart damage, is caused by decreased blood flow [ 1 ]. (biomedcentral.com)
Cardiac myocyte apoptosis may be induced by tumor necrosis factor-a, oxidative stress, atrial natriuretic peptide, hypoxia, and stretching. (latestfashiontips.com)
The downstream regulator of PI3K/Akt is hypoxia-inducible factor-1α (HIF-1α) which is a master regulator of gene expression in hypoxia, and it has the ability to influence cellular adaptive responses to hypoxia or ischemia. (springeropen.com)

Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. (silverchair.com)

Although intralipid inhibits the opening of the mitochondrial permeability transition pore as efficiently as cyclosporine-A, intralipid is more effective in reducing the infarct size and improving the cardiac functional recovery. (silverchair.com)

This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.com)
Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
The coronary arteries perfuse the cardiomyocytes located within the myocardium. (wikipedia.org)
Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured. (spandidos-publications.com)
Improved heart function was accompanied by reduced inflammation, including decreased cell-migration into the infarcted myocardium and improved cell survival in the infarct border zone as detected by reduced expression of pro-apoptotic proteins in the acute phase and reduced active caspase3 5 days after I/R. (isth.org)
Cell therapy is currently emerging as a potential new treatment for post MI patients with the assumption that recolonization of the areas of scarred myocardium with exogenously supplied surrogates or precursors of cardiomyocytes can restore function and ultimately affect clinical outcomes. (escardio.org)
and is an intrinsic process through which repeated short episodes of ischemia are instituted to protect the myocardium against subsequent ischemic insults [ 7 ]. (biomedcentral.com)
Apoptosis occurs in the infarcted area, border zone, and distal myocardium in acute myocardial infarction. (latestfashiontips.com)
Numerous studies have documented that cardiomyocyte apoptosis occurs in border zone of infarct scars and in the remote zone of non-infarcted myocardium [ 2 - 4 ], which exacerbates the post-MI remodeling and aggravates cardiac dysfunction [ 5 ]. (ijbs.com)

The re-establishing of blood flow to an ischemic zone is called reperfusion [ 1 ]. (biomedcentral.com)
Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
The degree of apoptotic cell death following ischemia/reperfusion may be reduced by the use of caspase inhibitors, antioxidants, and ischemic preconditioning. (latestfashiontips.com)
Hang P, Sun C, Guo J, Zhao J, Du Z. BDNF-mediates Down-regulation of MicroRNA-195 Inhibits Ischemic Cardiac Apoptosis in Rats. (ijbs.com)
The present study was performed to investigate the role of miR-195 and the interplay between BDNF and miR-195 in ischemic cardiomyocyte apoptosis. (ijbs.com)
miR-195 level was dynamically regulated in response to MI and significantly increased in ischemic regions 24 h post-MI as well as in hypoxic or H 2 O 2 -treated cardiomyocytes. (ijbs.com)
Up-regulation of miR-195 in ischemic cardiomyocytes promotes ischemic apoptosis by targeting Bcl-2. (ijbs.com)

Therefore, we designed this study to see the influence of atorvastatin on cardiomyocyte apoptosis and Fas expression following acute I/R in vivo. (ac.ir)
Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
Through this research, we will achieve a better understanding of the pathogenesis of acute cardiac injury during ischemia/reperfusion and post-infarct remodeling. (elsevierpure.com)
Acute kidney injury (AKI) can result from a variety of etiologies (e.g., ischemia, toxicity, and sepsis) and is characterized by high rates of morbidity and mortality. (biolifesas.org)
Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. (nature.com)
Apoptotic cardiomyocyte death is an increasingly recognized feature of congestive heart failure and acute myocardial infarction. (latestfashiontips.com)
Studies have also suggested that both acute substantial cardiomyocyte loss and chronic low levels of apoptosis contributed to the development of heart failure [ 6 , 7 ]. (ijbs.com)

The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
These protective effects may be associated with the inhibition of apoptosis and inflammation, as reflected by less TUNEL-positive cells and lower levels of serum proinflammatory cytokines (Interleukin-1β, Interleukin-6, tumor necrosis factor-α) and cardiac troponin I in the N-CM group compared with the vehicle group. (researchsquare.com)
Our results show that platelets modulate inflammation and cell-survival after myocardial infarction indicating platelet interaction with inflammatory and endothelial cells and migration into the infarcted border zone to induce cell apoptosis of cardiomyocytes and / or inflammatory leukocyte. (isth.org)
Silent information regulator transcript-1 (Sirt1) is a histone deacetylase that is nicotinamide adenine dinucleotide (NAD+) reliant and closely associated with several cellular processes, including cell metabolism, aging, apoptosis, inflammation, and oxidative stress [ 10 ]. (biomedcentral.com)
After 48 hours of exposure, these mice showed persistent cardiac inflammation and oxidative tissue damage that caused sarcomeric disruption, cardiomyocyte death, left ventricular dysfunction, and cardiomyopathy, while control hearts showed minimal damage. (jci.org)
The progression of cardiovascular diseases is usually associated with numerous stimuli, including ischemia, inflammation, and pressure or volume overload, all of which may induce cardiac fibrosis. (cyberleninka.org)

It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
We have observed this in adult cardiomyocytes in vitro and in the heart in vivo. (elsevierpure.com)
Parkin is known to inhibit cardiomyocyte death in vitro, and deletion of Parkin in vivo markedly exacerbates post-infarct remodeling, heart failure, and mortality. (elsevierpure.com)
In vivo, treatment of mice with rAAV9-BAG3 prior to I/R significantly decreased infarct size and improved left ventricular function when compared with mice receiving rAAV9-GFP and improved markers of autophagy and apoptosis. (uthscsa.edu)
Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)

Recent data suggested that microRNA-101a (miR-101a) exerted anti-fibrotic effects in post-infarct cardiac remodeling and improved cardiac function. (cyberleninka.org)

Upregulation of miR‑133b‑5p contributes to HPC‑mediated cardioprotection in cardiomyocytes, and the mechanism may be associated with inhibition of caspase‑8 and caspase‑3 apoptotic signaling. (spandidos-publications.com)
In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
It does not have the morphological characteristics of typical necrosis, such as swelling of the cytoplasm and organelles and rupture of the cell membrane, nor does it have the characteristics of traditional cell apoptosis, such as cell shrinkage, chromatin condensation, formation of apoptotic bodies and disintegration of the cytoskeleton. (nature.com)
The morphologic changes seen in apoptosis include cell shrinkage, loss of cell-cell contacts, membrane blebbing, and nuclear condensation, terminating in the breakdown of the cell into apoptotic bodies that are phagocytosed by surrounding cells. (latestfashiontips.com)
Activation of the mitochondrial apoptotic process is regarded as the point of no return in apoptosis. (latestfashiontips.com)
BDNF mitigated the pro-apoptotic effect of miR-195 in rat cardiomyocytes. (ijbs.com)

Nowadays, more and more studies have revealed that cells in the cardiovascular system (such as cardiomyocytes, vascular smooth muscle cells, endothelial cells, et al. (frontiersin.org)
These cells have been shown to have the capability of differentiating into cardiomyocytes, vascular smooth muscle cells, and endothelial cells. (biomedcentral.com)
These cells have the potential to differentiate into cardiovascular lineages, such as cardiomyocytes (CMs), endothelial cells (ECs), and vascular smooth muscle cells (VSMCs) [ 7 ]. (biomedcentral.com)

PLCA at 1 μM and metformin at 30 μM exerted similar effects on the improvement of cell viability and the alleviation of cell apoptosis in NRVM after H/R. PLCA promoted p-AMPK, p-AKT, and GLUT4 upregulation to induce a cardioprotective effect in both cell and animal model. (biomedcentral.com)
HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. (spandidos-publications.com)
Since cardiomyocytes are terminally differentiated cells with limited self-renewal capacity, and membrane rupture is a major cause of cardiomyocyte cell death following injury, membrane repair is a necessary process for preserving cardiomyocyte viability [ 6 ]. (biomedcentral.com)
Cell viability and apoptosis were detected by MTT assay and TdT-mediated dUTP nick end labeling (TUNEL) staining, respectively. (ijbs.com)
Apoptosis in both hypoxic and H 2 O 2 -treated cardiomyocytes were markedly reduced and cell viability was increased by miR-195 inhibitor. (ijbs.com)

Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)

Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)

Recent studies have shown that in addition to necrosis and apoptosis, there are also other new programmed death modes, such as autophagy, necrosis and necrotic apoptosis, which have unique biological processes and pathophysiological characteristics. (nature.com)

Cardiac ischemia is modelled in vitro through the application of hypoxic and oxidative stress. (biomedcentral.com)
To investigate this hypothesis, the H9c2 cardiomyocyte cell line was used to establish an in vitro myocardial H/R injury model to explore the roles and potential mechanisms of STA in myocardial H/R injury. (biomedcentral.com)

While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
Methods and Results: Two weeks following coronary artery occlusion in rats, the expression levels of both TGFpi and TGFpRI were increased, but the expression of miR-101a was decreased at the site of the infarct and along its border. (cyberleninka.org)

The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
Additionally, machine reperfusion induces the production of ROS, which results in I/R injury to the heart. (gotomydoctor.com)
ATP1B2 is certainly portrayed higher in glioblastoma stem-like cells (GSCs) than in GBM cells and its own Rabbit Polyclonal to NPM downregulation induces apoptosis of GSCs. (tech-strategy.org)

Accordingly, the over-arching hypothesis of this project is that Bax and Parkin antagonize each other for the benefit of cardiomyocytes: The binding of Bax, likely in its cell death-inactive conformation, to Parkin inhibits Parkin-mediated mitophagy to prevent mitochondrial depletion. (elsevierpure.com)
However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
Mitochondrial involvement in apoptosis is evidenced by the loss of the mitochondrial membrane, opening of mitochondrial transition pores, disruption of the electron transport chain, generation of reactive oxygen species, and translocation of cytochrome cto the cytoplasm, where it activates caspases. (latestfashiontips.com)
The hemodynamic function, infarct size, calcium retention capacity, mitochondrial superoxide production, and phosphorylation levels of protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) were measured. (silverchair.com)
HO-1) pathway was tested for defense of mitochondrial quality control in cardiomyocyte-specific Hmox1 KO mice (HO-1[CM] -/- ) exposed to oxidative stress (100% O 2 ). (jci.org)
However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.com)
Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)

However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)

The accumulation of cardiac lactate was attenuated by PLCA during myocardial I/R, and infarct size was smaller in rats treated with PLCA (1 mg/kg) than in those treated with caffeic acid (1 mg/kg). (biomedcentral.com)
Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
Adeno-associated viral (AAV)-NRP-1 was stereotaxically inoculated into the cortex and ipsilateral striatum posterior of adult male Sprague-Dawley (SD) rats before a 90-min transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion. (biomedcentral.com)
Cardiac function and apoptosis were detected in MI rats intravenously injected with antagomiR-195. (ijbs.com)
Meanwhile, BDNF protein level was rapidly increased in MI rats and H 2 O 2 -treated cardiomyocytes. (ijbs.com)
Ischemia was induced in male (M-Isch) and female (F-Isch) rats with sc. (biomedcentral.com)

IPC activates the reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways to protect the heart against IR injury. (biomedcentral.com)
Our previous studies suggested that brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) axis inhibited cardiomyocyte apoptosis in myocardial infarction (MI). (ijbs.com)

The deleterious effects of H/R on apoptosis and autophagy were recapitulated by knockdown of BAG3 with Ad-siBAG3 and were rescued by Ad-BAG3. (uthscsa.edu)

A prior research indicated which the 3 subunit (ATP1B3) is normally overexpressed in gastric cancers, and its own downregulation induced significant cancers cell apoptosis [35]. (tech-strategy.org)

A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
Intramyocardial injections of saline (n = 5), microrods (n = 7), decorin microrods (n = 10), and free decorin (n = 4) were performed in male rat models of ischemia-reperfusion MI to evaluate therapeutic effects on cardiac remodeling and function. (bvsalud.org)
Gal-3C profoundly benefitted left ventricular ejection fraction, end-systolic and end-diastolic volumes, haemodynamic parameters, infarct scar size, and interstitial fibrosis, with better therapeutic efficacy than losartan and spironolactone monotherapies over the 56-day study. (bvsalud.org)
These findings suggest that BAG3 may provide a therapeutic target in patients undergoing reperfusion after myocardial infarction. (uthscsa.edu)

In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)

Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. (elifesciences.org)
Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. (elifesciences.org)
In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. (elifesciences.org)
This study provides important findings on the distinct functions of resident and recruited macrophages during cardiac healing after myocardial ischemia. (elifesciences.org)
Using state-of-the-art fate-mapping models and genetic and pharmacological targeting approaches, the authors provide solid evidence that the absence of resident macrophages do not influence infarct size but instead alter the immune cell crosstalk in response to injury. (elifesciences.org)

In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
While altered BAG3 expression has been associated with cardiac dysfunction, its role in ischemia/reperfusion (I/R) is unknown. (uthscsa.edu)
However, questions remain as to whether apoptosis is a critical event in the transition from compensated to decompensated cardiac hypertrophy and the onset of ventricular dysfunction. (latestfashiontips.com)

Current methods of cold static storage have reached their limits in storage time due to the extent of ischemia-reperfusion (I/R) injury induced during static cold storage. (gotomydoctor.com)
The extent of reperfusion injury is directly proportional to preservation time in cold storage, and research has shown that with static storage methods, heart storage time will not exceed six hours. (gotomydoctor.com)

Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)
Short-term cardiac stress, induced by ischemia-reperfusion (I/R) injury resulted in impaired left ventricular (LV) recovery and increased infarct size in heterozygous Hmox1-deficient (Hmox1 +/− ) mice [ 55 ]. (springer.com)
MG53 KO mice lack IPC-mediated cardioprotection as evidenced by a failure of IPC to reduce IR-induced myocardial infarct size. (biomedcentral.com)
This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. (elifesciences.org)
Cardiac function, histology, and infarct size were assessed, and inflammatory markers quantified by RT-PCR. (biomedcentral.com)
At day 7, infarct size was increased by cigarette smoking in males only, which was accompanied by enhanced collagen deposition in both the infarcted and peri-infarcted areas. (biomedcentral.com)

Vascular endothelial cell (EC)-derived factors play an important role in endothelial-cardiomyocyte crosstalk and could save cardiomyocytes (CMs) from injury. (mdpi.com)

Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
STA significantly suppressed oxidative stress, reduced MDA content, and increased SOD activity in H9c2 cells exposed to H/R. STA reduced apoptosis in H9c2 cells exposed to H/R, as evidenced by the reduced TUNEL positive cells and caspase-3 activity. (biomedcentral.com)

For instance, some studies have suggested that in addition to antioxidant enzymes, nitric oxide synthases (NOSs), and other traditional enzymes, novel molecular targets such as mitochondria-targeting hydrogen sulfide (H 2 S) donor AP39 and its auxiliary targets have recently been identified as critical participants in H 2 S synthesis for modulating the postischemic cardiomyocyte survival in a manner independent of classical cytosolic signaling mechanisms [ 7 , 8 ]. (hindawi.com)
Upon myocardial infarction (MI) immune system becomes activated by extensive necrosis of cardiomyocytes and release of damage-associated molecular patterns [ 16 ]. (springer.com)
q g Investigations and research Advances in cardiovascular molecular imaging: the case of Annexin A5 Apoptosis helps identify patients at risk of stroke or myocardial infarction. (abcdocz.com)

H9c2 rat cardiomyocyte cell line was obtained from the American Type Culture Collection (Manassas, VA, USA. (spandidos-publications.com)

has been demonstrated to attenuate renal ischemia‑reperfusion (I/R) injury. (spandidos-publications.com)

Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
Given the directness of the connection between Bax and cardiomyocyte apoptosis and necrosis, however, we challenge that view and hypothesize that Parkin protects the heart primarily through its inhibition of Bax. (elsevierpure.com)
We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.com)

These examples indicate that the ability to image apoptosis could improve the diagnosis and treatment of patients with cardiovascular disease. (abcdocz.com)
In this article we briefly discuss the opportunities for using Annexin A5 for the non-invasive detection of apoptosis in patients with cardiovascular disease. (abcdocz.com)

Cells were pretreated with STA (50 µM) 2 h before H/R. Cardiomyocyte injury was evaluated by CCK-8 assay and lactate dehydrogenase (LDH) release. (biomedcentral.com)

However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. (biomedcentral.com)
Therefore, the study aimed to investigate the protective effects and mechanisms of STA on H/R injury of cardiomyocytes. (biomedcentral.com)

With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
In recent years, extensive research has established that some immune cells either reside in the heart or have very complicated interactions with cardiomyocytes through permanent blood circulation. (biomedcentral.com)
In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
The resistant state of skeletal myoblasts to ischemia renders these cells suitable candidates for repair of chronically infracted and failing heart (5). (escardio.org)
What is the pathophysiologic significance of cardiomyocyte apoptosis in heart failure? (latestfashiontips.com)
Thus, successfully reversal of cardiomyocyte apoptosis during early stage of MI is crucial for repairing the injured heart and ameliorating cardiac function [ 8 ]. (ijbs.com)

Cell apoptosis occurs, such as by activation of caspase-3 activity, and finally leads to myocardial infarction [ 1 ]. (biomedcentral.com)
oxidative stress that occurs during reperfusion injury has been shown to induce apoptosis, over and above that induced by ischemia. (latestfashiontips.com)

Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
Interestingly, contradictory data exist for transformation of bone marrow derived progenitor cells (BMPC) into new cardiomyocytes and alternative mechanisms as enhanced neovascularization, enhanced scar tissue formation due to augmented inflammatory response and decreased apoptosis have been suggested for the benefical effects of these cells on myocardial function after myocardial infarction (4). (escardio.org)

Conversely, the Bax-Parkin interaction inhibits Bax, likely through interfering with its transition to its active conformation, thereby inhibiting cardiomyocyte apoptosis and necrosis. (elsevierpure.com)
Our data speculated that STA protects H/R injury and inhibits oxidative stress and apoptosis in cardiomyocytes by activation of the SIRT1-Nrf2 pathway. (biomedcentral.com)

miR‑133b‑5p antagomir was transfected into the cardiomyocytes to observe whether it could block HPC‑induced cardioprotection. (spandidos-publications.com)
However, the knockdown of miR‑133b‑5p in the cardiomyocytes blocked HPC‑mediated cardioprotection as reflected by the aggravation of cell injury and apoptosis. (spandidos-publications.com)

Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. (nature.com)

There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. (archivesofmedicalscience.com)

We postulate that this is a physiological mechanism that restrains inappropriate or excessive elimination of mitochondria, a situation that would be deleterious to cardiomyocytes, which are highly dependent on ATP. (elsevierpure.com)

Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest, to a lack of sensation or paralysis that could require amputation. (wikipedia.org)

Unlike cell necrosis, apoptosis does not elicit an inflammatory response, and plasma membrane integrity is maintained until late in the process. (latestfashiontips.com)

Cell survival during ischemia/reperfusion is governed by HIF-1α-dependent genes such as heme oxygenase-1, inducible nitric oxide synthase, cyclooxygnease-2, and vascular endothelial growth factor. (springeropen.com)

In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. (archivesofmedicalscience.com)
Our study has highlighted sex-specific alterations in systolic and diastolic function shortly after ischemia, and provided a comprehensive look at the underlying proteomic changes and the influence of estrogens and their metabolites. (biomedcentral.com)

Klier M, Ayhan A, Dannenberg L, Gorressen S, Polzin A, Elvers M. Role of Platelets in Processes of Myocardial Healing After Myocardial Ischemia and Reperfusion in Mice [abstract]. (isth.org)

Apoptosis was assessed by TUNEL staining and caspase-3 activity. (biomedcentral.com)

Anatomy26

Organisms12

Diseases36

Chemicals and Drugs108

Analytical, Diagnostic and Therapeutic Techniques and Equipment35

Phenomena and Processes42

Disciplines and Occupations1

Health Care2

Reduced infarct size2

Hypoxia11

Subjected to ischemia followed by reperfusion2

Reducing the infarct size1

Myocardium10

Ischemic7

Acute7

Inflammation6

Vivo5

Post-infarct1

Apoptotic7

Endothelial cells3

Viability5

Inhibit cardiomyocyte1

Cardioprotective1

Necrosis and apoptosis1

Vitro2

Coronary artery4

Induces3

Mitochondrial7

Myocardial reperfusion1

Rats6

Kinase2

Autophagy1

Downregulation1

Therapeutic4

Pathways1

Macrophages5

Dysfunction4

Methods2

Size6

Crosstalk1

Significantly2

Molecular3

H9c21

Attenuate1

Protects the heart3

Cardiovascular2

Lactate1

Protective2

Heart6

Occurs2

Mechanisms2

Inhibits2

Cardioprotection2

Pathophysiological1

Progenitor cells1

Mitochondria1

Arterial1

Inflammatory response1

Survival1

Function2

Mice1

Caspase-3 activity1