ArticleCell death and differentiation2015
E2F1-regulated miR-30b suppresses Cyclophilin D and protects heart from ischemia/reperfusion injury and necrotic cell death.
Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Pooled it
- Cardiac SR-Mitochondria Contacts-Impact on Cardiac Physiology and Mitochondrial Fitness.Cells · 2025Review
- The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025Review
- Comprehensive bioinformatics analysis and experimental verification identify mitochondrial gene Dgat2 as a novel therapeutic biomarker for myocardial ischemia-reperfusion.Frontiers in endocrinology · 2025Article
- The role of mitochondria-associated ER membranes in disease pathology: protein complex and therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- Non-Coding RNA-Mediated Gene Regulation in Cardiovascular Disorders: Current Insights and Future Directions.Journal of cardiovascular translational research · 2024Review
- H3K27ac acts as a molecular switch for doxorubicin-induced activation of cardiotoxic genes.Clinical epigenetics · 2024Article
- LncRNA MALAT1 suppresses monocyte-endothelial cell interactions by targeting miR-30b-5p and enhancing ATG5-mediated autophagy.Heliyon · 2024Article
- Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial Function.Circulation · 2024Article
- Modeling Cardiotoxicity in Pediatric Oncology Patients Using Patient-Specific iPSC-Derived Cardiomyocytes Reveals Downregulation of Cardioprotective microRNAs.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- MicroRNA-155-5p in serum derived-exosomes promotes ischaemia-reperfusion injury by reducing CypD ubiquitination by NEDD4.ESC heart failure · 2023Article
- Repositioning linifanib as a potent anti-necroptosis agent for sepsis.Cell death discovery · 2023Article
- Interdependent Nuclear Co-Trafficking of ASPP1 and p53 Aggravates Cardiac Ischemia/Reperfusion Injury.Circulation research · 2023Article
- A bibliometric analysis of myocardial ischemia/reperfusion injury from 2000 to 2023.Frontiers in cardiovascular medicine · 2023Review
- Exosomes Derived from E2F1International journal of nanomedicine · 2023Article
- Mitochondria-associated endoplasmic reticulum membranes (MAMs): Possible therapeutic targets in heart failure.Frontiers in cardiovascular medicine · 2023Review
- Emerging Role of MicroRNA-30c in Neurological Disorders.International journal of molecular sciences · 2022Review
- Cell death regulation by MAMs: from molecular mechanisms to therapeutic implications in cardiovascular diseases.Cell death & disease · 2022Review
- Characterization and Validation of ceRNA-Mediated Pathway-Pathway Crosstalk Networks Across Eight Major Cardiovascular Diseases.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease remains the leading cause of morbidity and mortality worldwide. Cell death is a hallmark characteristic of various cardiac diseases, including myocardial infarction and heart failure. Emerging evidences suggest that necrosis is programmed and is one of the main forms of cell death in the pathological process in cardiac diseases. However, the molecular components regulating programmed necrosis in heart remain largely unidentified. Here we report that miR-30b, Cyclophilin D (CypD) and E2F1 constitute an axis that regulates necrosis. The results show that knockdown of CypD attenuated necrosis in the cellular model and also myocardial infarction in the animal model. miR-30b suppresses the translation of CypD and thus inhibits CypD-mediated necrotic cell death in cardiomyocytes. Cardiac-specific miR-30b transgenic mice exhibit reduced necrosis and myocardial infarct size upon ischemia/reperfusion (I/R) injury. Further, we identify that E2F1 transcriptionally represses miR-30b expression. Knockdown of E2F1 in cardiomyocytes inhibits necrotic cell death, and E2F1 knockout mice show reduced necrosis and myocardial infarct size upon I/R. Our present study identifies a novel signaling pathway composed of E2F1, miR-30b and CypD that regulates myocardial necrosis. This discovery will not only provide de novo regulators in the necrotic process but will also shed new light on the effective therapy of myocardial infarction and heart failure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.