Heart mitochondria and calpain 1: Location, function, and targets.
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Summary
Inhibition of the mit-CPN1 could be a potential strategy to decrease cardiac injury during ischemia-reperfusion, especially in pathophysiological conditions.
- Type
- review
- Published
- 2015-11-01
- Cited by
- 45
- References
- 100
- OpenAlex
- https://openalex.org/W1438230784
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:205806768
Keywords
Intermembrane space, Calpain, Mitochondrial intermembrane space, Mitochondrion, Cell biology
References
- Calpain-Mediated Impairment of Na+/K+–ATPase Activity During Early Reperfusion Contributes to Cell Death After Myocardial Ischemia
- Over-expression of calpastatin inhibits calpain activation and attenuates myocardial dysfunction during endotoxaemia.
- Calpain translocation and activation as pharmacological targets during myocardial ischemia/reperfusion.
- New era of calpain research
- Identification of p53 in mitochondria.
- Calpain: novel family members, activation, and physiologic function.
- Ischemia-reperfusion-induced changes in sarcolemmal Na+/K+-ATPase are due to the activation of calpain in the heart.
- The role of autolysis in activity of the Ca2+-dependent proteinases (mu-calpain and m-calpain).
- Activation of mitochondrial‐u‐calpain sensitizes opening of the mitochondrial permeability transition pore during ischemia‐reperfusion (648.11)
- Nitric oxide inhibition of cytochrome oxidase and mitochondrial respiration: Implications for inflammatory, neurodegenerative and ischaemic pathologies
- Mitochondrial calcium uptake
- Reversible Blockade of Electron Transport during Ischemia Protects Mitochondria and Decreases Myocardial Injury following Reperfusion
- Apoptosis-Inducing Factor: Structure, Function, and Redox Regulation
- Four types of calpastatin isoforms with distinct amino-terminal sequences are specified by alternative first exons and differentially expressed in mouse tissues.
- Mediation of Poly(ADP-Ribose) Polymerase-1-Dependent Cell Death by Apoptosis-Inducing Factor
- Muscle-specific calpain, p94, interacts with the extreme C-terminal region of connectin, a unique region flanked by two immunoglobulin C2 motifs.
- Calpain system and its involvement in myocardial ischemia and reperfusion injury.
- Calpain activation induced by glucose deprivation is mediated by oxidative stress and contributes to neuronal damage.
- Release of mitochondrial cytochrome c and activation of cytosolic caspases induced by myocardial ischaemia.
- High glucose-induced Ca2+ overload and oxidative stress contribute to apoptosis of cardiac cells through mitochondrial dependent and independent pathways.
Cited by
- Activation of mitochondrial calpain and increased cardiac injury: beyond AIF release.
- Potential Roles of Humanin on Apoptosis in the Heart.
- Increased level of phosphorylated desmin and its degradation products in heart failure
- Mitochondrial Metabolism in Aging Heart
- Mitochondrial Ca2+ and Regulation of the Permeability Transition Pore
- Up-regulation of junctophilin-2 prevents ER stress and apoptosis in hypoxia/reoxygenation-stimulated H9c2 cells
- Eryptosis in Haemochromatosis: Implications for rheology
- بررسی تغییرات نوکلئوتیدی ژنهای میتوکندریایی ATP6، ND3 و COX3 در بیماران مبتلا به پلاکهای آترواسکلروتیک با روش PCR-SSCP
- Cell Death Mechanisms in a Mouse Model of Retinal Degeneration in Spinocerebellar Ataxia 7.
- Cardiac Specific Knockout of p53 Decreases ER Stress-Induced Mitochondrial Damage
- Increased calpain-1 in mitochondria induces dilated heart failure in mice: role of mitochondrial superoxide anion
- Adipose tissue-derived autotaxin causes cardiomyopathy in obese mice.
- Inhibition of the ubiquitous calpains protects complex I activity and enables improved mitophagy in hearts following ischemia-reperfusion.
- The study of mitochondrial ATP6, ND3 and COX3 gene nucleotide variations in Iranian patients with atherosclerosis by PCR-SSCP
- Endoplasmic Reticulum Stress-induced Complex I Defect: Central Role of Calcium Overload
- Inhibition of GPR35 Preserves Mitochondrial Function After Myocardial Infarction by Targeting Calpain 1/2
- Endoplasmic reticulum stress-mediated mitochondrial dysfunction in aged hearts.
- Cardiomyocyte Specific Deletion of p53 Decreases Cell Injury During Ischemia-Reperfusion: Role of Mitochondria
- Targeted inhibition of calpain in mitochondria alleviates oxidative stress-induced myocardial injury
- Calpain Activation and Organ Failure in Sepsis: Molecular Insights and Therapeutic Perspectives
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