ArticleInternational journal of molecular sciences2020
Programmed Cell Death in the Left and Right Ventricle of the Late Phase of Post-Infarction Heart Failure.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Necrosis-like cell death modes in heart failure: the influence of aetiology and the effects of RIP3 inhibition.Basic research in cardiology · 2025Article
- PANoptosis: a potential target of cardiomyopathy.Frontiers in immunology · 2025Review
- MAO-B inhibition by selegiline blunts cardiac functions improved by high-fat diet: Role of inflammation, apoptosis, and calcium-handling.Current research in pharmacology and drug discovery · 2025Article
- Mechanisms and Therapeutic Potential of Multiple Forms of Cell Death in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2024Review
- Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences.Physiological research · 2024Review
- Mitral regurgitation severity at left ventricular assist device implantation is associated with distinct myocardial transcriptomic signatures.The Journal of thoracic and cardiovascular surgery · 2023Article
- Cardiac Reverse Remodeling in Ischemic Heart Disease with Novel Therapies for Heart Failure with Reduced Ejection Fraction.Life (Basel, Switzerland) · 2023Review
- Molecular Mechanisms of Mitochondrial Quality Control in Ischemic Cardiomyopathy.International journal of biological sciences · 2023Review
- Hypertension and Cardiovascular Diseases: From Etiopathogenesis to Potential Therapeutic Targets.International journal of molecular sciences · 2022Article
- Interplay of Oxidative Stress and Necrosis-like Cell Death in Cardiac Ischemia/Reperfusion Injury: A Focus on Necroptosis.Biomedicines · 2022Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
While necroptosis has been shown to contribute to the pathogenesis of post-infarction heart failure (HF), the role of autophagy remains unclear. Likewise, linkage between these two cell death modalities has not been sufficiently investigated. HF was induced by 60-min left coronary occlusion in adult Wistar rats and heart function was assessed 6 weeks later followed by immunoblotting analysis of necroptotic and autophagic proteins in both the left (LV) and right ventricle (RV). HF had no effect on RIP1 and RIP3 expression. PhosphoSer229-RIP3, acting as a pro-necroptotic signal, was increased in LV while deceased in RV of failing hearts. Total MLKL was elevated in RV only. Decrease in pSer555-ULK1, increase in pSer473-Akt and no significant elevation in beclin-1 and LC3-II/I ratio indicated rather a lowered rate of autophagy in LV. No beclin-1 upregulation and decreased LC3 processing also suggested the inhibition of both autophagosome formation and maturation in RV of failing hearts. In contrast, p89 PARP1 fragment, a marker of executed apoptosis, was increased in RV only. This is the first study showing a different signaling in ventricles of the late phase of post-infarction HF, highlighting necroptosis itself rather than its linkage with autophagy in LV, and apoptosis in RV.
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Registered trials
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