• Mitochondrial ATP synthase catalyzes ATP synthesis, utilizing an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation. (wikipedia.org)
  • Mitochondrial function or the ability to generate energy through OXPHOS (oxidative phosphorylation) is vital for cell homeostasis and its dysfunction has been linked to the pathogenesis of nearly all chronic diseases ( Pieczenik and Neustadt, 2007 ). (frontiersin.org)
  • Glutaredoxin-2 is Required to Control Oxidative Phosphorylation in Cardiac Muscle by Mediating Deglutathionylation Reactions. (ohri.ca)
  • In addition, different cell types exhibit preference for specific metabolic pathways (fatty acid oxidation/FAO, glycolysis or oxidative phosphorylation/OxPhos). (upenn.edu)
  • Cellular respiration (oxidative phosphorylation) occurs in the mitochondria, where a series of enzymes catalyze the transfer of electrons to molecular oxygen and the generation of energy-storing adenosine triphosphate (ATP). (msdmanuals.com)
  • Tissues with a high energy demand (eg, brain, nerves, retina, skeletal and cardiac muscle) are particularly vulnerable to defects in oxidative phosphorylation. (msdmanuals.com)
  • Increase in the lactate:pyruvate ratio distinguishes oxidative phosphorylation defects from other genetic causes of lactic acidosis. (msdmanuals.com)
  • Mutations in the ND5 subunit of complex I of the mitochondrial DNA are a frequent cause of oxidative phosphorylation disease. (cdc.gov)
  • Altogether, these results indicate that the inability to enhance myofilament relaxation through cTnI phosphorylation predisposes the heart to abnormal diastolic function, reduced accessibility of cardiac reserves, dysautonomia, and hypertrophy. (fsu.edu)
  • A pathological cardiac hypertrophy model, junctate-1 transgenic mice and control mice, were analyzed using label-free quantitative phosphoproteomics to identify differentially phosphorylated proteins and sites. (molcells.org)
  • Changes in phosphorylation levels of Ser-98 and Ser-179 in Ldb3 were further confirmed in NRVMs and other pathological/physiological hypertrophy models, including transverse aortic constriction and swimming models, using site-specific phospho-antibodies. (molcells.org)
  • Cardiac hypertrophy can be characterized as the response of the heart to various hemodynamic stresses. (molcells.org)
  • Although cardiac hypertrophy is initiated by various receptors at cell membranes sensing biomechanical signals and hormones, it is generally mediated by cellular signaling cascades. (molcells.org)
  • In cardiac hypertrophy, phosphorylation-dependent functional modulation of proteins, especially sarcoplasmic reticulum (SR) and sarcomere proteins, has been demonstrated. (molcells.org)
  • Plasma prorenin and aldosterone levels were determined in 4-wk intervals, and cardiac marker enzymes for hypertrophy, fibrosis, and oxidative stress as well as cardiac pathology were investigated. (nih.gov)
  • In the heart, decreased proteolytic capacity and accumulating proteotoxcity have been shown to directly exacerbate outcomes in cardiac infarcts, hypertrophy, and failure 9 , 10 . (nature.com)
  • Phosphorylation of the chromatin remodeling factor DPF3a induces cardiac hypertrophy through releasing HEY repressors from DNA. (mpg.de)
  • Long term ablation of protein kinase A (PKA)-mediated cardiac troponin I phosphorylation leads to excitation-contraction uncoupling and diastolic dysfunction in a knock-in mouse model of hypertrophic cardiomyopathy. (fsu.edu)
  • The cardiac troponin I (cTnI) R21C (cTnI-R21C) mutation has been linked to hypertrophic cardiomyopathy and renders cTnI incapable of phosphorylation by PKA in vivo. (fsu.edu)
  • Ca 2+ desensitization of myofilaments is indicated as a primary mechanism for the pathogenesis of familial dilated cardiomyopathy (DCM) associated with the deletion of lysine 210 (ΔK210) in cardiac troponin T (cTnT). (elsevierpure.com)
  • Cardiac Myosin Binding Protein-C (cMyBPC) and cardiac troponin I (cTNI) are hypertrophic cardiomyopathy (HCM)-causing sarcomeric proteins which regulate contractility in response to PKA phosphorylation. (biomedcentral.com)
  • Cardiac troponin I (cTnI) is the inhibitory Subunit of cardiac troponin, a key myofilament regulatory protein complex located on the thin filaments of the contractile apparatus. (agu.edu.tr)
  • Phosphorylation levels of cardiac troponin I (cTnI) were determined by Western blot. (cdc.gov)
  • This review discusses troponin as a marker of cardiac injury, its testing, utility, appropriateness use criteria, and interpretation of abnormal values. (medscape.com)
  • The 99th percentile cutoff point for cardiac troponin T (cTnT) is well-known at 0.01 ng/mL (with 10% coefficient of variance value at the 99th percentile of 0.03 ng/mL), as only one cTnT assay exists. (medscape.com)
  • The 99th percentile of a reference decision limit (medical decision cutoff) for cardiac troponin (cTn) assays should be determined in each local laboratory with internal studies using the specific assay that is used in clinical practice or validating a reference interval that is based on findings in the literature. (medscape.com)
  • For PCI in patients with normal baseline troponin values, elevations of cardiac biomarkers above the 99th percentile upper reference limit indicate periprocedural myocardial necrosis. (medscape.com)
  • An initial small elevation occurs when troponins are released from the cytosolic pool, when troponin molecules in the cytosol of cardiac muscle diffuse across the sarcolemma into the surrounding lymphatics and blood vessels, becoming detectable in blood. (medscape.com)
  • Cardiac myocytes isolated from older R21C mice demonstrate that in the presence of isoproterenol, significant delays in Ca(2+) decay and sarcomere relaxation occur that are not present at 6 months of age. (fsu.edu)
  • It has previously been demonstrated that phosphatidylinositol‑3‑kinase (PI3K)/Akt and cleaved caspase‑3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. (spandidos-publications.com)
  • Epigallocatechin‑3‑gallate (EGCG), the predominant catechin component of green tea, has been reported to have potential cardioprotective effects in primary cultures of cardiac myocytes exposed to I/R injury, mediated through inhibition of signal transducers and activators of transcription‑1 activity. (spandidos-publications.com)
  • Since EGCG + Zn2+ may, at least in part, protect cardiac myocytes against H/R‑induced apoptotic cell death, the PI3K/Akt pathway of EGCG may be enhanced by its interactions with zinc during H/R injury. (spandidos-publications.com)
  • Previous studies have identified apoptosis as a significant mechanism underlying cell death during I/R injury in cultured cardiac myocytes ( 6 , 7 ), and that the inhibition of this apoptosis is able to prevent I/R injury ( 8 ). (spandidos-publications.com)
  • In addition, Townsend et al ( 12 ) reported that EGCG reduced signal transducers and activators of transcription-1 phosphorylation and protected cardiac myocytes against I/R-induced apoptotic cell death in isolated rat hearts. (spandidos-publications.com)
  • We show that PDE4D gene inactivation in mice results in a progressive cardiomyopathy, accelerated heart failure after myocardial infarction, and cardiac arrhythmias. (nih.gov)
  • However, numerous studies have demonstrated that light to moderate alcohol consumption (ie, 1-2 drinks per day or 3-9 drinks per week) decreases the risk of cardiac events such as myocardial infarction. (medscape.com)
  • The novel mechanism of action on cellular compartments has been found continually, which opens a new way for their potential application in cardiac failure and other cardiac events like post-myocardial infarction. (benthamscience.com)
  • Recently, EndMT has been increasingly recognized as a vital process that contributes to various cardiovascular pathologies in adults, which include atherosclerosis, valvular heart disease, cardiac fibrosis, and myocardial infarction. (dovepress.com)
  • Analysis of cardiac myofibrils isolated from ΔK210 hearts identified a decrease in phosphorylation of cTnI (46%), cTnT (30%) and MyBP-C (32%) compared with wild-type controls. (elsevierpure.com)
  • Interestingly, immunoblot analyses with phospho-specific antibodies show augmented phosphorylation of cTnT-Thr 203 (28%) and decreased phosphorylation of cTnI-Ser 23/24 (41%) in mutant myocardium. (elsevierpure.com)
  • In vitro kinase assays indicate that ΔK210 increases phosphorylation propensity of cTnT-Thr 203 three-fold, without changing cTnI-Ser 23/24 phosphorylation. (elsevierpure.com)
  • This study ascribes a novel function to MMGL isoform 4: it meets all criteria for classification as an AKAP, and we show that is involved in the phosphorylation of cMyBPC as well as cTNI, hence MMGL is an important regulator of cardiac contractility. (biomedcentral.com)
  • cTnI is uniquely specific for the heart and is widely used in clinics as a serum biomarker for cardiac injury. (agu.edu.tr)
  • Phosphorylation of cTnI plays a critical role in modulating cardiac function. (agu.edu.tr)
  • However, a comprehensive characterization of phosphorylation of mouse cTnI occurring in vivo has been lacking. (agu.edu.tr)
  • Herein, we have employed top-down mass spectrometry (MS) methodology with electron capture dissociation for precise mapping of in vivo phosphorylation sites of cTnI affinity purified from wild-type and transgenic mouse hearts, As demonstrated, top-down MS (analysis of intact proteins) is an extremely valuable technology for global characterization of labile phosphorylation occurring in vivo without a priori knowledge. (agu.edu.tr)
  • Our top-down MS data unambiguously identified Ser22/23 as the only two sites basally phosphorylated in wild-type mouse cTnI with full sequence coverage, which was confirmed by the lack of phosphorylation in cTnI-Ala(2) transgenic mice where Ser22/23 in cTnI have been rendered nonphosphorylatable by mutation to alanine. (agu.edu.tr)
  • Phosphorylation levels of cTnI in the left ventricle were significantly lower at d 1 postexposure. (cdc.gov)
  • Cardiomyocyte alterations observed after welding fume treatment were mainly due to alterations in intracellular calcium handling and phosphorylation levels of cTnI. (cdc.gov)
  • The aim of the present study was to test the hypothesis that elevation of prorenin in plasma is sufficient to induce cardiac fibrosis. (nih.gov)
  • We found that prorenin and aldosterone alone are not sufficient to induce considerable cardiac fibrosis in the absence of sodium load. (nih.gov)
  • Activin receptor-like kinase 7 silencing alleviates cardiomyocyte apoptosis, cardiac fibrosis, and dysfunction in diabetic rats. (nih.gov)
  • Endothelial-to-mesenchymal transition (EndMT) is an important mechanism underlying cardiac fibrosis. (dovepress.com)
  • This study aimed to investigate the possible effect of TMZ on cardiac fibrosis exerted via the inhibition of NOX2-mediated EndMT. (dovepress.com)
  • A cardiac fibrosis model was established in Sprague-Dawley rats through a subcutaneous injection of isoproterenol (ISO, 5 mg/kg/d). (dovepress.com)
  • Rats injected with ISO exhibited severe interstitial cardiac fibrosis and perivascular fibrosis, decreased left ventricular ejection fraction, and increased NOX activity. (dovepress.com)
  • TMZ treatment mitigated cardiac fibrosis, ameliorated left ventricular dysfunction, and reduced NOX activity. (dovepress.com)
  • TMZ may ameliorate EndMT and ISO-induced cardiac fibrosis through the NOX2/NF-κB/Snail pathway. (dovepress.com)
  • The findings of the study may provide new insights into the potential role of TMZ in the pathophysiology of cardiac fibrosis. (dovepress.com)
  • Myocardial fibrosis, characterized as interstitial fibroblast proliferation and excessive collagen deposition, is the structural basis of myocardial stiffness and the key process of cardiac function transformation from the compensatory phase to heart failure. (dovepress.com)
  • Cardiac fibroblasts are generally the primary effector cells of fibrosis and have been reported to be partly derived from cardiac endothelial cells through the endothelial to mesenchymal transition (EndMT) process. (dovepress.com)
  • Recent developments in mass spectrometry-based phosphoproteomics have led to the identification of thousands of differentially phosphorylated proteins and their phosphorylation sites. (molcells.org)
  • However, functional studies of these differentially phosphorylated proteins have not been conducted in a large-scale or high-throughput manner due to a lack of methods capable of revealing the functional relevance of each phosphorylation site. (molcells.org)
  • Considerable evidence supports the proposition that phosphorylation of cardiac sarcomeric proteins is a key modulator of function and may exacerbate the effect of the deletion. (elsevierpure.com)
  • In this study we investigate the impact of K210 deletion on phosphorylation propensity of sarcomeric proteins. (elsevierpure.com)
  • Cardiac contractility is regulated by dynamic phosphorylation of sarcomeric proteins by kinases such as cAMP-activated protein kinase A (PKA). (biomedcentral.com)
  • Efficient phosphorylation requires that PKA be anchored close to its targets by A-kinase anchoring proteins (AKAPs). (biomedcentral.com)
  • Cardiac myosin binding protein-C (cMyBP-C) is one of the proteins that make up the contractile apparatus of cardiomyocytes. (scirp.org)
  • Using an integrated platform of metabolic labeling, high-resolution mass spectrometry and computational analysis, we report here a comprehensive dataset of the in vivo half-life of 3,228 and the expression of 8,064 cardiac proteins, quantified under healthy and hypertrophic conditions across six mouse genetic strains commonly employed in biomedical research. (nature.com)
  • The dataset contains over 1.92 million data points in protein isotope labeling kinetics, culminating as the in vivo turnover rates of 3,228 cardiac proteins and the expression levels of 8,064 proteins. (nature.com)
  • The results showed that cardiac maCh-R consist of two subclasses, both regulated by GTP binding proteins. (nii.ac.jp)
  • It is possible that M2 and M2 come from dif-ferent modification of receptor proteins, such as phosphorylation, methylation, association with other protein or polymerization. (nii.ac.jp)
  • PDE4D3 levels in the RyR2 complex were reduced in failing human hearts, contributing to PKA-hyperphosphorylated, "leaky" RyR2 channels that promote cardiac dysfunction and arrhythmias. (nih.gov)
  • Cardiac arrhythmias and dysfunction associated with PDE4 inhibition or deficiency were suppressed in mice harboring RyR2 that cannot be PKA phosphorylated. (nih.gov)
  • Additionally, it may clinically manifest with myocardial necrosis, cardiac arrhythmia, myocardial stunning and microvascular dysfunction ( 5 ). (spandidos-publications.com)
  • Targeting RyR2 with a phosphorylation site-specific nanobody reverses dysfunction of failing cardiomyocytes in rats. (bvsalud.org)
  • Chronic PKA phosphorylation of ryanodine receptor 2 ( RyR2 ) has been shown to increase diastolic sarcoplasmic reticulum (SR) Ca2+ leakage and lead to cardiac dysfunction. (bvsalud.org)
  • In patients, PDE inhibitors have been linked to heart failure and cardiac arrhythmias, although the mechanisms are not understood. (nih.gov)
  • Schlossarek, S., Mearini, G. and Carrier, L. (2011) Cardiac myosin-binding protein c in hypertrophic cardiomyopathy: Mechanisms and therapeutic opportunities. (scirp.org)
  • Therefore, spinal AMPA receptor phosphorylation contributes to the mechanisms underlying stress-induced pain transition. (jneurosci.org)
  • Pulmonary exposure to different welding fumes may exert a negative impact on cardiac function, although the underlying mechanisms remain unclear. (cdc.gov)
  • Keystone Symposium, Molecular Mechanisms of Cardiac Disease and Regeneration, February 19-24. (anl.gov)
  • Both exercise-induced molecular mechanisms and physiological cardiac remodeling have been previously studied on a whole heart level. (researchgate.net)
  • Mechanisms regulating cardiomyocyte cell cycle arrest are of great interest partly because reversing this process could provide a way to stimulate cardiac regeneration after injury [ 17 ]. (springer.com)
  • These results indicate that P-light chain phosphorylation affects actin-myosin interactions in cardiac and skeletal muscles at submaximal levels of Ca 2+ activation. (elsevierpure.com)
  • Sweeney, HL & Stull, JT 1986, ' Phosphorylation of myosin in permeabilized mammalian cardiac and skeletal muscle cells ', American Journal of Physiology - Cell Physiology , vol. 250, no. 4 (19/4), pp. (elsevierpure.com)
  • Barefield, D. and Sadayappan, S. (2010) Phosphorylation and function of cardiac myosin-binding protein c in health and disease. (scirp.org)
  • The phosphodiesterase 4D3 (PDE4D3) was found in the cardiac ryanodine receptor (RyR2)/calcium-release-channel complex (required for excitation-contraction [EC] coupling in heart muscle). (nih.gov)
  • Phosphorylation of P-light chain increased tension in both permeabilized cardiac and skeletal muscle fibers. (elsevierpure.com)
  • Troponins are protein molecules that are part of cardiac and skeletal muscle. (medscape.com)
  • A cell-based functional assay system measuring hypertrophic cell growth of neonatal rat ventricle cardiomyocytes (NRVMs) following phenylephrine treatment was applied, and changes in phosphorylation of individual differentially phosphorylated sites were induced by incorporation of phosphorylation competition peptides conjugated with cell-penetrating peptides. (molcells.org)
  • By profiling the transcriptome of ~24,000 nuclei, we identified major and rare cardiac cell types and revealed significant heterogeneity of cardiomyocytes, fibroblasts, and endothelial cells in postnatal developing hearts. (upenn.edu)
  • For instance, neurons rely on glycolysis and ensuing OxPhos but not FAO, while cardiomyocytes use OxPhos and FAO to generate most energy for cardiac contraction. (upenn.edu)
  • Moreover, AR185 gene transfer inhibited the PKA-mediated phosphorylation of RyR2 in failing cardiomyocytes . (bvsalud.org)
  • Cell-based functional screening against 18 selected phosphorylation sites identified three phosphorylation sites (Ser-98, Ser-179 of Ldb3, and Ser-1146 of palladin) displaying near-complete inhibition of cardiac hypertrophic growth of NRVMs. (molcells.org)
  • As part of the "flight or fight" response, protein kinase A phosphorylates phospholamban (PLN), thereby relieving a tonic inhibition of the endo/sarco-plasmic reticulum calcium pump, which results in an increased force of cardiac contraction. (elifesciences.org)
  • Atrial fibrillation (AF) is the most common form of cardiac arrhythmia. (nature.com)
  • Atrial fibrillation is the most common type of cardiac arrhythmia, and is responsible for substantial morbidity and mortality in the general population. (nature.com)
  • 7. Uncontrolled intercurrent illnesses including, but not limited to: active infections, symptomatic congestive heart failure, unstable angina pectoris, cardiac arrhythmia, Diabetes Mellitus and/or psychiatric illness involving the incompetence of the subject. (who.int)
  • Mesenchymal stem cells secrete factors that inhibit apoptosis in H9c2 cardiac myoblasts. (anl.gov)
  • PLN interacts with sarco/endoplasmic reticulum Ca 2+ -ATPase (SERCA) and regulates calcium uptake, which is modulated by the protein kinase A (PKA)-dependent phosphorylation of PLN during the fight-or-flight response. (elifesciences.org)
  • Publications] Y. Watanabe: 'Effect of phosphorylation of inhibitory GTP-binding protein by cyclic AMP-dependent protein kinase on its ADP-ribosylation by pertussis toxin, islet-activating protein. (nii.ac.jp)
  • We hypothesize that intracellular gene delivery of an RyR2 -targeting phosphorylation site-specific nanobody could preserve the contractility of the failing myocardium . (bvsalud.org)
  • To initiate cardiac muscle contraction, an action potential depolarizes the sarcolemma and activates the voltage-gated calcium channel, Ca V 1.2, which mediates Ca 2+ influx ( Bers, 2002 ). (elifesciences.org)
  • Our structures, combined with the results from other biophysical and biochemical assays, reveal a common disease mechanism: the mutations in PLN reduce its phosphorylation level by changing its conformation and weakening its interactions with PKA. (elifesciences.org)
  • Our results provide preclinical experimental evidence that the cardiac expression of RyR2 nanobodies with AAV9 vectors is a promising therapeutic strategy for HF. (bvsalud.org)
  • Cardiac mitochondrial function is altered in a variety of inherited and acquired cardiovascular diseases. (jci.org)
  • When applied to a mouse model of pediatric mitochondrial cardiomyopathy, we uncovered profound cell type-specific modifications of the cardiac transcriptional landscape at single-nucleus resolution, including changes of subtype composition, maturation states, and functional remodeling of each cell type. (upenn.edu)
  • Taken together, CITED4 expression is necessary for exercise-induced regional remodeling of the heart's microstructural helicity revealing how a key molecular regulator of cardiac remodeling manifests into downstream local tissue-level changes. (researchgate.net)
  • Expression of transcription factor CITED4 is necessary for exercise-induced regional remodeling of the heart's microstructural helicity, revealing how a key molecular regulator of cardiac remodeling mediates local tissue-level changes. (researchgate.net)
  • Originally thought to have only a structural role, cMyBPC has been shown to play an important role in the regulation of cardiac contractility [ 1 ], for which the N-terminal region of the protein appears to be crucial. (biomedcentral.com)
  • Publications] X.M. Zhou: 'The SH-H subgroup of cardiac M_2 receptors (M_2 ) inhibits adenulate cyclase activity. (nii.ac.jp)
  • Publications] A. Mizushima: 'The H-L subgroup of guinea-pig cardiac M_2 receptors (M_2 ) regulates formation of inositol phosphates. (nii.ac.jp)
  • More importantly, we are using proximity labeling in vivo to identify and understand new heart-derived hormones in physiology and disease, a new area of research of cardiac endocrinology. (upenn.edu)
  • the cardiac isoform differs from its skeletal counterparts by containing an extra immunoglobulin-like (IgI) domain (C0) at the amino terminal, a charged residue-rich insertion in domain C5 and three phosphorylation sites in a motif between the second and third IgI domains (C1-C2), known as the MyBPC motif or m-domain. (biomedcentral.com)
  • Bone marrow mesenchymal stem cells secrete factors that exert anti-apoptotic and pro-apoptotic effects on H9c2 cardiac myoblasts. (anl.gov)
  • In the present study, the protective effects of EGCG with zinc were assessed on cultures of rat cardiac myoblasts exposed to hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
  • To explore the effect of welding fumes on cardiac function, Sprague-Dawley rats were exposed by intratracheal instillation to 2 mg/rat of manual metal arc hard surfacing welding fume (MMA-HS) once per week for 7 wk. (cdc.gov)
  • To our knowl edge there are no antibodies commercially availa ble for phosphorylated cMyBP-C. Thus, the p-PKD- Ser744/748 antibody can accelerate research into th e role of cMyBP-C phosphorylation in cardiomyo cytes. (scirp.org)
  • In 2005, he founded the MGH Cardiac Metabolic Syndrome Program in the Cardiovascular Disease Prevention Center. (massgeneral.org)
  • Cardiac Endocrinology: Heart-derived hormones in physiology and disease. (upenn.edu)
  • 2. Single cell multiomics to understand metabolic and cardiac biology and disease. (upenn.edu)
  • Funded with several NIH and DOD grants, we are currently applying single-cell multiomics to understand metabolic and cardiac biology and disease. (upenn.edu)
  • Keystone Symposium, Molecular Pathways in Cardiac Development and Disease, January 22-27. (anl.gov)
  • Molecular modeling of cTnT-ΔK210 structure reveals changes in the electrostatic environment of cTnT helix (residues 203-224) that lead to a more basic environment around Thr 203 , which may explain the enhanced PKC-dependent phosphorylation. (elsevierpure.com)
  • Therefore, this new post-translational modification of ERK5 could be a very important process to regulate both endothelial and cardiac physiology, especially in diabetic conditions. (mdanderson.org)
  • Marrow-derived mesenchymal stem cells ( MSC ) express cardiac specific protein in co-culture. (anl.gov)
  • Incubation of permeabilized cardiac fibers from R21C mice with PKA confirmed that the mutation prevents facilitation of mechanical relaxation. (fsu.edu)
  • Keystone Symposium, Molecular Biology of Cardiac Diseases and Regeneration, April 3-8. (anl.gov)
  • Additionally, to further elucidate the function of MMGL, we used it as bait to screen a cardiac cDNA library. (biomedcentral.com)
  • Phosphorylation of cMyBP-C is essential for normal cardiac function, since dephosphorylation of this protein leads to its degradation and has been associated with cardiomyopathy. (scirp.org)
  • While studying HDAC inhibitors in cardiac function, Dr. Mahesh Gupta's laboratory showed that acetylation is important for sarcomere function. (cytoskeleton.com)
  • In patients undergoing CABG or PCI in whom baseline cardiac enzyme values are abnormal, it is difficult to confirm periprocedural MI. (medscape.com)
  • Observations during the second half of the 19th century described cardiac enlargement seen at autopsy and heart failure symptoms in persons who had consumed excessive amounts of alcohol. (medscape.com)
  • Nonischaemic dilated cardiomyopathy (NIDCM) is one of the most common inherited cardiomyopathy and is considered to be one of the main causes of heart failure and sudden cardiac death. (hindawi.com)
  • We investigated the potential of adeno-associated virus (AAV)9-mediated cardiac expression of AR185 to combat postischemic heart failure (HF). (bvsalud.org)
  • Coronary sinus, normally located between the LEFT ATRIUM and LEFT VENTRICLE on the posterior surface of the heart, can serve as an anatomical reference for cardiac procedures. (bvsalud.org)