ArticleJournal of cellular and molecular medicine2019
Different signalling in infarcted and non-infarcted areas of rat failing hearts: A role of necroptosis and inflammation.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Z-DNA-binding protein 1 exacerbates myocardial ischemia‒reperfusion injury by inducing noncanonical cardiomyocyte PANoptosis.Signal transduction and targeted therapy · 2025Article
- Necrosis-like cell death modes in heart failure: the influence of aetiology and the effects of RIP3 inhibition.Basic research in cardiology · 2025Article
- Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences.Physiological research · 2024Review
- Is Intrinsic Cardioprotection a Laboratory Phenomenon or a Clinically Relevant Tool to Salvage the Failing Heart?International journal of molecular sciences · 2023Review
- Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Review
- Analysis of Signaling Pathways of Necroptotic and Pyroptotic Cell Death in the Hearts of Rats With Type 2 Diabetes Mellitus.Physiological research · 2023Article
- Hydrogen sulfide protects against ischemic heart failure by inhibiting RIP1/RIP3/MLKL-mediated necroptosis.Physiological research · 2022Article
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
- Necroptosis at a glance.Journal of cell science · 2022Article
- Necroptosis in heart disease: Molecular mechanisms and therapeutic implications.Journal of molecular and cellular cardiology · 2022Review
- Analysis of necroptosis and its association with pyroptosis in organ damage in experimental pulmonary arterial hypertension.Journal of cellular and molecular medicine · 2022Article
- Interplay of Oxidative Stress and Necrosis-like Cell Death in Cardiac Ischemia/Reperfusion Injury: A Focus on Necroptosis.Biomedicines · 2022Review
- Quercetin alleviates diastolic dysfunction and suppresses adverse pro-hypertrophic signaling in diabetic rats.Frontiers in endocrinology · 2022Article
- Mitochondrial A-kinase anchoring proteins in cardiac ventricular myocytes.Physiological reports · 2021Article
- Inhibition of Cardiac RIP3 Mitigates Early Reperfusion Injury and Calcium-Induced Mitochondrial Swelling without Altering Necroptotic Signalling.International journal of molecular sciences · 2021Article
- Programmed cell death in stem cell-based therapy: Mechanisms and clinical applications.World journal of stem cells · 2021Review
- Targeting necroptosis as therapeutic potential in chronic myocardial infarction.Journal of biomedical science · 2021Review
- The Molecular Mechanisms of Iron Metabolism and Its Role in Cardiac Dysfunction and Cardioprotection.International journal of molecular sciences · 2020Review
- Programmed Cell Death in the Left and Right Ventricle of the Late Phase of Post-Infarction Heart Failure.International journal of molecular sciences · 2020Article
- Neutrophil-Mediated Cardiac Damage After Acute Myocardial Infarction: Significance of Defining a New Target Cell Type for Developing Cardioprotective Drugs.Antioxidants & redox signaling · 2020Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis has been recognized in heart failure (HF). In this study, we investigated detailed necroptotic signalling in infarcted and non-infarcted areas separately and its mechanistic link with main features of HF. Post-infarction HF in rats was induced by left coronary occlusion (60 minutes) followed by 42-day reperfusion. Heart function was assessed echocardiographically. Molecular signalling and proposed mechanisms (oxidative stress, collagen deposition and inflammation) were investigated in whole hearts and in subcellular fractions when appropriate. In post-infarction failing hearts, TNF and pSer229-RIP3 levels were comparably increased in both infarcted and non-infarcted areas. Its cytotoxic downstream molecule p-MLKL, indicating necroptosis execution, was detected in infarcted area. In non-infarcted area, despite increased pSer229-RIP3, p-MLKL was present in neither whole cells nor the cell membrane known to be associated with necroptosis execution. Likewise, increased membrane lipoperoxidation and NOX2 levels unlikely promoted pro-necroptotic environment in non-infarcted area. Collagen deposition and the inflammatory csp-1-IL-1β axis were active in both areas of failing hearts, while being more pronounced in infarcted tissue. Although apoptotic proteins were differently expressed in infarcted and non-infarcted tissue, apoptosis was found to play an insignificant role. p-MLKL-driven necroptosis and inflammation while inflammation only (without necroptotic cell death) seem to underlie fibrotic healing and progressive injury in infarcted and non-infarcted areas of failing hearts, respectively. Upregulation of pSer229-RIP3 in both HF areas suggests that this kinase, associated with both necroptosis and inflammation, is likely to play a dual role in HF progression.
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Registered trials
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