• The findings of the present study indicated that inhibition of miR‑132 may ameliorate myocardial I/R injury by inhibiting oxidative stress and pyroptosis through activation of PGC‑1α/Nrf2 signalling by targeting SIRT1. (spandidos-publications.com)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • METHODS AND RESULTS: Stabilization of myocardial HIF-1 was achieved by pharmacological inhibition of prolyl hydroxylase (PHD) domain-containing enzyme using GSK360A or using cardiac-specific ablation of von Hippel-Lindau protein (VHL(fl/fl)) in mice. (ox.ac.uk)
  • One of the primary causes of ARF is ischemia/reperfusion (I/R). Inflammatory process and oxidative stress are thought to be the major mechanisms causing I/R. MK-886 is a potent inhibitor of leukotrienes biosynthesis which may have anti-inflammatory and antioxidant effects through inhibition of polymorphonuclear leukocytes (PMNs) infiltration into renal tissues. (biomedcentral.com)
  • discovered that constant infusion of MB counteracts early myocardial dysfunction and derangement of hemodynamics and gas exchange by inhibition of nitric oxide pathway within an ovine endotoxemia model [48]. (immune-source.com)
  • Inhibition of Na+/H+ exchange is protective against ischemic injury, while inhibition of the vacuolar ATPase promotes apoptosis, in part by shifting the proton load toward the Na+/H+ transporter and thus increasing Ca2+ uptake, and in part by reducing the myocyte capacity to control [pH]i. (biomedres.us)
  • 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)
  • These findings were further confirmed when HIF-1 stabilization in the rat and murine heart resulted in smaller myocardial infarct sizes (both in vivo and ex vivo), decreased mitochondrial oxidative stress, and inhibited MPTP opening following IRI, effects which were also found to be dependent on HKII. (ox.ac.uk)
  • In this study, we hypothesized that STA could attenuate myocardial H/R injury. (biomedcentral.com)
  • Bone marrow mesenchymal stem cells (BMSCs) have been reported to attenuate myocardial I/R injury via their paracrine effects, which can be enhanced by hypoxic preconditioning. (researchsquare.com)
  • The nitric oxide donor S-nitroso-human-serum-albumin (S-NO-HSA) is known to attenuate myocardial ischemia-reperfusion (I/R)-injury. (frontierspartnerships.org)
  • leaves alleviate hypoxia/reoxygenation (H/R) injury in H9c2 cardiomyocytes and to explore potential mechanisms. (hindawi.com)
  • In murine cardiomyocytes miR-21 was found to protect from hypoxia/reoxygenation (H/R)-induced cell apoptosis via regulation of its target gene PDCD4 [ 13 ]. (hindawi.com)
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.com)
  • Vascular endothelial cell (EC)-derived factors play an important role in endothelial-cardiomyocyte crosstalk and could save cardiomyocytes (CMs) from injury. (mdpi.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • 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)
  • Therefore, the study aimed to investigate the protective effects and mechanisms of STA on H/R injury of cardiomyocytes. (biomedcentral.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)
  • However, the role of STA on the H/R injury of cardiomyocytes through the SIRT1-Nrf2 pathway remains unexplored. (biomedcentral.com)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Methods and Results-In vitro, neonatal rat cardiomyocytes were subjected to hypoxia-reoxygenation in the absence or presence of eEPCs with or without Tβ4 short hairpin RNA (shRNA) transfection. (elsevierpure.com)
  • Besides, the of PARP and caspase 3 protein, the level of reactive oxygen species (ROS), and mitochondrial membrane potentials under hypoxia were compared between groups for more confirmation. (shsmu.edu.cn)
  • Research progress in myocardial ischemia-reperfusion injury mediated by mitochondrial reactive oxygen species [J]. JOURNAL OF SHANGHAI JIAOTONG UNIVERSITY (MEDICAL SCIENCE), 2021, 41(6): 826-829. (shsmu.edu.cn)
  • This article reviews the anti-inflammatory relative and anti-infectious effects of Evodia rutaecarpa and its major bioactive components and the involvement of the nitric oxide synthases, cyclooxygenase, NADPH oxidase, nuclear factor kappa B, hypoxia-inducible factor 1 alpha, reactive oxygen species, prostaglandins, tumor necrosis factor, LIGHT, amyloid protein and orexigenic neuropeptides. (biomedcentral.com)
  • Becker LB. New concepts in reactive oxygen species and cardiovascular reperfusion physiology. (jamanetwork.com)
  • During tourniquet-related ischemia, aerobic respiration stops, and ATP is depleted, and during subsequent reperfusion, there is an increase in reactive oxygen species (ROS) production and other endogenous substances, which leads to acute ischemia-reperfusion (IR) injuries, including tissue necrosis and skeletal muscle contractile dysfunction. (nebraska.edu)
  • The key mechanisms underlying myocardial I/R injury include increased intracellular calcium concentration, sudden generation of reactive oxygen species (ROS) and inflammatory cytokines, adenosine triphosphate (ATP) depletion, and development of metabolic acidosis. (researchsquare.com)
  • The myocardial I/R model was established using C57BL/J6 mice. (spandidos-publications.com)
  • Adult male mice (ICR) were adapted to intermittent hypobaric hypoxia 8 hours per day, 5 days per week for 5 weeks. (nusl.cz)
  • 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)
  • CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. (engreen.com.cn)
  • A total of 24 Adult males of Swiss albino mice were randomized to four groups: I/R group (n = 6), mice underwent 30 minute bilateral renal ischemia and 48 hr reperfusion. (biomedcentral.com)
  • Sham group (n = 6), mice underwent same anesthetic and surgical procedures except for ischemia induction. (biomedcentral.com)
  • After the end of reperfusion phase mice were sacrificed, blood samples were collected directly from the heart for determination of serum TNF-a, IL-6, urea and Creatinine. (biomedcentral.com)
  • Here, we studied the protective effects of HBO pretreatment with 100% oxygen at 2.5 ATA against tourniquet/IR injury in mice. (nebraska.edu)
  • After one hour of HBO therapy with 100% oxygen at 2.5 ATA was administered to C57/BL6 mice, a rubber band was placed at the hip joint of the unilateral hindlimb to induce 3 h of ischemia and then released for 48 h of reperfusion. (nebraska.edu)
  • Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)
  • 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)
  • 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)
  • The in vitro I/R model was established by the hypoxia/reoxygenation method using H9C2 cells. (spandidos-publications.com)
  • The molecular mechanism was further determined by examining the effects of PD98059, a specific inhibitor of the ERK signaling pathways in H9C2 cells with hypoxia/reoxygenation treatment. (engreen.com.cn)
  • H9c2 cells were exposed to 8 h hypoxia (1% O2) followed by 18 h reoxygenation, after which cell viability was assessed by monitoring mitochondrial reduction of MTT, lactate dehydrogenase release and caspase-3 activation. (ntu.ac.uk)
  • These results have shown that A1 adenosine receptor and β2-adrenoceptor-induced protection against simulated hypoxia/reoxygenation occurs in a TG2 and Gi/o-protein dependent manner in H9c2 cardiomyoblasts. (ntu.ac.uk)
  • Rat cardiomyocyte H9c2 cells underwent H/R (hypoxia for 4 h and reoxygenation for 12 h). (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)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • 3. Agomir-503 treatment worsens hypoxia/reoxygenation-induced injuries, while antagomir-503 treatment attenuates them and increases phosphorylation of Stat3 (Y705) and Akt (T450). (fullpicture.app)
  • Pharmacological pre- and post-conditioning with CPA and isoprenaline significantly reduced hypoxia/reoxygenation-induced cell death. (ntu.ac.uk)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.com)
  • Recent studies have demonstrated that supplementation of nitric oxide (NO), or increased expression of endothelial NO-synthase (eNOS) protects against both IR-injury and fibrosis ( 5 , 6 ). (frontierspartnerships.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)
  • Murine models of Matrigel plug and hindlimb ischemia were employed as in vivo angiogenic assays. (biomedcentral.com)
  • MB research in ischemic heart stroke While low-dose MB has been shown to lessen neurobehavioral impairment in neurodegenerative illnesses (Parkinson's disease [23 29 Alzheimer disease [30-32]) the neuroprotective ramifications of MB on cerebral ischemia in vivo had been only. (immune-source.com)
  • citation needed] While some investigations suggest a possible beneficial effect of mesenchymal stem cells on heart and kidney reperfusion injury, to date, none have explored the role of stem cells in muscle tissue exposed to ischemia-reperfusion injury. (wikipedia.org)
  • 1. MicroRNA-503 (miR-503) exacerbates myocardial ischemia/reperfusion (I/R) injury by inhibiting prosurvival signaling pathways, including PI3K/Akt and STAT3. (fullpicture.app)
  • 6 3 In fact, one of the first pieces of evidence for a role of succinate in cancer development was provided by the discovery of pseudohypoxia, which refers to activation of hypoxia signaling pathways under normal oxygen levels. (haematologica.org)
  • The results support significant roles for miR-126 in regulating cardiac myocyte survival pathways and cell death during exposure to simulated ischemia and acidosis. (biomedres.us)
  • Thus, although Txnip deletion suppresses mitochondrial function, protection from myocardial ischemia is enhanced as a result of a coordinated shift to enhanced anaerobic metabolism, which provides an energy source outside of mitochondria. (jci.org)
  • Autophagy represents a general homeostatic and inducible adaptive response to environmental stress, including endoplasmic reticulum stress, hypoxia, oxidative stress, and exposure to pharmaceuticals and xenobiotics. (houstonmethodist.org)
  • Therefore, exploring new therapeutic agents and investigating their potential mechanisms underlying myocardial H/R injury is important. (biomedcentral.com)
  • Commercial kits were used to measure the levels of serum myocardial enzymes and inflammatory factors. (spandidos-publications.com)
  • Apparent histologic injury and elevated levels of serum myocardial enzymes and inflammatory factors were observed in the myocardial I/R model. (spandidos-publications.com)
  • Myocardial I/R injury may induce cell apoptosis and autophagy by activating oxidative stress and upregulating inflammatory mediators, ultimately resulting in irreversible fibrotic damage ( 3 ). (spandidos-publications.com)
  • Abouzaki NA, Christopher S, Trankle C, Van Tassell BW, Carbone S, Mauro AG, Buckley L, Toldo S and Abbate A: Inhibiting the inflammatory injury after myocardial ischemia reperfusion with plasma-derived Alpha-1 Antitrypsin: A post hoc analysis of the VCU-α1RT study. (spandidos-publications.com)
  • Here we investigated roles for miR-126 in stress kinase activation, induction of inflammatory cytokines and apoptosis caused by exposure of cultured cardiac myocytes to hypoxia/acidosis or acidosis alone. (biomedres.us)
  • Important roles of inflammatory mediators in cardiac cell death by ischemia with or without reperfusion are well established [12-14]. (biomedres.us)
  • Nevertheless, it is not known if EPO induced by chronic hypoxia plays a role in its cardioprotective mechanism. (nusl.cz)
  • The results indicate that exogenous EPO employs the same cardioprotective mechanisms as adaptation to chronic intermittent hypoxia. (nusl.cz)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • citation needed] Tissue swelling and fasciotomy Following ischemia, reperfusion induces local tissue swelling. (wikipedia.org)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • Conversely, blocking miR-21 expression with miR-21 inhibitor effectively suppressed the protective effects of TFs against H/R-induced injury. (hindawi.com)
  • The aim of this study was to find out if protective effect of exogenous EPO adds up to protection offered by chronic hypoxia. (nusl.cz)
  • Inflammation is a protective physiological response of an organism to chemical, physical, infectious agents, environmental toxins, ischemia or an antigen-antibody interaction. (biomedcentral.com)
  • Stachydrine (STA), an active constituent of Leonurus heterophyllus sweet, could have a protective effect on myocardial H/R injury, which remains unexplored. (biomedcentral.com)
  • We assessed whether donor preservation with S-NO-HSA affects isograft injury and myocardial expression of GATA2 as well as miR-126-3p, which are considered protective against vascular and endothelial injury. (frontierspartnerships.org)
  • Subarachnoid haemorrhage (SAH) is one of the most severe forms of stroke in which delayed cerebral ischemia is one of the major complications. (biomedcentral.com)
  • Chronic hypoxia in the presence of high glucose leads to progressive acidosis of cardiac myocytes in culture. (biologists.com)
  • Adaptation to chronic hypoxia increases myocardial resistance to acute ischemia/reperfusion (I/R) injury, similarly to application of exogenous erythropoietin (EPO). (nusl.cz)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • Chronic allograft injury (CAI), consisting of vasculopathy and interstitial fibrosis, affects approximately 50% of patients after 10 years and limits long-term survival following heart transplantation ( 1 ). (frontierspartnerships.org)
  • Our group reported that severe chronic hypoxia alone does not cause apoptosis of cardiac myocytes in culture. (biomedres.us)
  • The objective of present study was to assess the effects of MK-886 and DITPA on renal I/R injury. (biomedcentral.com)
  • Acute kidney injury (AKI) is a common clinical syndrome characterized by rapid deterioration of renal function. (biomedcentral.com)
  • Preclinical studies have identified autophagy as a process that can be activated during vascular disorders, including ischemia - reperfusion injury of the heart and other organs, cardiomyopathy, myocardial injury, and atherosclerosis. (houstonmethodist.org)
  • It has been reported that SIRT1/peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α/nuclear factor erythroid-2-related factor 2 (Nrf2) signalling can mediate oxidative stress, which plays an important role in myocardial I/R injury ( 14 , 15 ). (spandidos-publications.com)
  • miR‑132 was significantly upregulated and SIRT1 was markedly downregulated in I/R myocardial tissues. (spandidos-publications.com)
  • The results indicated that TFs significantly alleviate H/R injury, which include inhibiting apoptosis and enhancing antioxidant capacity. (hindawi.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)
  • 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)
  • Despite the recent surge about miRNA discoveries for cardiac I/R injury, there is still very little known about the mechanism details because of the complexity of cellular events and the interference of other risk factors. (hindawi.com)
  • and the underlying mechanism of CLU4A in myocardial ischemia/reperfusion injury needs to be investigated. (engreen.com.cn)
  • In order to fully understand the mechanisms of I/R injury and to find novel therapeutic strategies, further research is stilled urgently needed [ 3 ]. (hindawi.com)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • Therapeutic hypothermia (TH) aims to ameliorate further injury in infants with moderate and severe hypoxic ischemic encephalopathy (HIE). (nature.com)
  • HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore. (ox.ac.uk)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • Acute coronary syndrome (ACS) is a cardiovascular disease, which describes any condition characterized by signs and symptoms of sudden myocardial ischaemia and reduction in blood flow to the heart [ 1 ]. (hindawi.com)
  • Myocardial ischemia, also called cardiac ischemia or hypoxia/reoxygenation (H/R)-induced heart damage, is caused by decreased blood flow [ 1 ]. (biomedcentral.com)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
  • Protection of the heart against injury from acute ischemia remains challenging for emergency physicians and cardiologists because there are no therapies proven to directly protect the heart against the deleterious effects of ischemia in humans. (mcw.edu)
  • 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)
  • Therefore, attenuating myocardial I/R injury during the heart transplant procedure would have a favorable impact on improving short- and long-term graft function and recipient's survival(6). (researchsquare.com)
  • Methylene blue provides been shown to boost blood circulation pressure and myocardial function by inhibiting nitric oxide activities in individual septic surprise disease [41 47 50 52 These research Zotarolimus showed that methylene blue provides vascular results and causes vasoconstriction transiently thus improving blood circulation pressure that could help to reduce the chances of hypoperfusion during heart stroke. (immune-source.com)
  • Obligatory roles for acidosis in promoting apoptosis confirmed our previous reports that hypoxia alone does not confer a lethal signal. (biomedres.us)
  • Acidosis with or without hypoxia increased apoptosis that was paralleled by elevated miR-126, increased phosphorylation of p38-MAPK and JNK, enhanced expression of IL-6, IL-8, and TNF, and downregulation of Bcl-2. (biomedres.us)
  • A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. (spandidos-publications.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)
  • Acute coronary syndrome (ACS) describes any condition characterized by myocardial ischaemia and reduction in blood flow. (hindawi.com)
  • We aimed to investigate the effect of PLCA on hypoxia/reoxygenation (H/R) in neonatal rat ventricular myocytes (NRVM) and on myocardial I/R in rats. (biomedcentral.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)
  • Background-Prolonged myocardial ischemia results in cardiomyocyte loss despite successful revascularization. (elsevierpure.com)
  • Once reperfusion occurs, these cellular products are returned to the systemic circulation, and are exposed to other organs. (wikipedia.org)
  • In pathological conditions, damaged cells transfer dysfunctional mitochondria toward recipient cells to ask for help and take up exogenous functional mitochondria to alleviate injury. (frontiersin.org)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • Hyperbaric oxygen (HBO) therapy can increase the arterial oxygen tension in the tissues of patients with general hypoxia/anoxia, including carbon monoxide poisoning, circulatory arrest, and cerebral and myocardial ischemia. (nebraska.edu)
  • Donor pre-treatment with S-NO-HSA lead to reduced fibrosis and preservation of myocardial miR-126-3p and GATA2 levels in murine cardiac isografts 60 days after transplantation. (frontierspartnerships.org)
  • Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. (medscape.com)
  • 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)
  • We have reported that retrograde application of embryonic endothelial progenitor cells (eEPCs) provides rapid paracrine protection against ischemia-reperfusion injury. (elsevierpure.com)
  • Organs involved in filtration (e.g., the kidneys and the liver), may be overwhelmed by the high load of cellular break down products, and face injury themselves (e.g., acute kidney injury). (wikipedia.org)
  • Molecular oxygen: friend and foe: the role of the oxygen free radical system in the calcium paradox, the oxygen paradox and ischemia/reperfusion injury. (jamanetwork.com)
  • However, few studies have focused on the role of miR-132 in myocardial I/R injury and the underlying mechanisms. (spandidos-publications.com)
  • Previous studies have shown that ischemia/reperfusion (I/R) injury acts as a significant role in PGD(4), contributing to adverse short- and long-term clinical outcomes in the recipients. (researchsquare.com)
  • Beneficial role of oleuropein in sepsis-induced myocardial injury. (ooir.org)
  • Recent evidence obtained in mouse models shows its essential role regulating blood cell function through various mechanisms that include pseudohypoxia responses by hypoxia-inducible factor-1α activation, post-translational modifications like succinylation, and communication mediated by succinate receptor 1. (haematologica.org)