ArticleFrontiers in cardiovascular medicine2022
Mitofilin Mitigates Myocardial Damage in Acute Myocardial Infarction by Regulating Pyroptosis of Cardiomyocytes.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- cIAP2-mediated IGF2BP2 ubiquitination and degradation regulate cardiomyocyte apoptosis via stabilizing mCell biology and toxicology · 2025Article
- Kaempferol inhibits cardiomyocyte pyroptosis via promoting O-GlcNAcylation of GSDME and improved acute myocardial infarction.BMC pharmacology & toxicology · 2025Article
- Mitofilin-mtDNA Axis Mediates Chronic Lead Exposure-Induced Synaptic Plasticity Impairment of Hippocampal and Cognitive Deficits.Biomolecules · 2025Article
- Therapeutic Potential of Gasdermin D-Mediated Myocardial Pyroptosis in Ischaemic Heart Disease: Expanding the Paradigm From Bench to Clinical Insights.Journal of cellular and molecular medicine · 2025Review
- Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.American journal of cardiovascular disease · 2025Review
- Pyroptosis in health and disease: mechanisms, regulation and clinical perspective.Signal transduction and targeted therapy · 2024Review
- The Role of Pyroptosis in Coronary Heart Disease.Anatolian journal of cardiology · 2024Article
- Leucine Supplementation Prevents the Development of Skeletal Muscle Dysfunction in a Rat Model of HFpEF.Cells · 2024Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute myocardial infarction (AMI) can lead to sudden cardiac death after prolonged ischemia or heart failure (HF) and impaired left ventricular pump function. However, the underlying mechanism remains largely unknown. The purpose of this study was to investigate the role of mitofilin in alleviating AMI. Methods: Recombinant adenoviral vectors for mitofilin overexpression or mitofilin knockdown were constructed, respectively. A mouse AMI model was established and the effect of mitofilin on myocardial pyroptosis was examined by detecting the lactate dehydrogenase (LDH) level and inflammatory factors. Moreover, a cellular model of AMI was established by treating cardiomyocytes with hypoxia/reoxygenation (H/R). An enzyme-linked immunosorbent assay (ELISA) and a western blot analysis were used to detect the effect of mitofilin knockdown on the expression of pyroptosis-related factors. Furthermore, the regulatory role of mitofilin in PI3K/AKT pathway was evaluated by the western blot and PI3K inhibitor. Results: Mitofilin was downregulated in the heart tissue of the AMI mice and H/R induced cardiomyocytes. The overexpression of mitofilin significantly alleviated AMI and reduced pyroptosis-related factors. Meanwhile, in cardiomyocytes, mitofilin knockdown aggravated cellular damages by promoting pyroptosis. Further analysis showed that the anti-pyroptotic effect of mitofilin was dependent on the activation of the PI3K/AKT signaling pathway. Conclusions: Our study suggests that mitofilin regulates pyroptosis through the PI3K/AKT signaling pathway in cardiomyocytes to ameliorate AMI, which may serve as a therapeutic strategy for the management of AMI.
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