ArticleThe journal of physiological sciences : JPS2019
Mst1 promotes cardiac ischemia-reperfusion injury by inhibiting the ERK-CREB pathway and repressing FUNDC1-mediated mitophagy.
Article in The journal of physiological sciences : JPS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 120 citations in OpenAlex.
- Article
- The mechanism of dexmedetomidine regulation of the HIF-1α/FUNDC1 axis in myocardial ischemia/reperfusion injury.Histology and histopathology · 2025Article
- Sex differences in cardiac graft recovery and pathophysiologic changes in a rat model of donation after circulatory death.Scientific reports · 2025Article
- LncRNA AK020546 Alleviates Myocardial Ischemia-Reperfusion Injury via Suppressing METTL14/m6A/MST1 Axis-Mediated Ferroptosis.Cardiovascular toxicology · 2025Article
- Crosstalk between MST1-Hippo and Wnt/β-Catenin, Notch, and PI3K/Akt pathways in cardiac physiology and pathology.Journal of physiology and biochemistry · 2025Review
- N6-methyladenosine readerWorld journal of gastroenterology · 2025Article
- Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- The correlation between mitochondria-associated endoplasmic reticulum membranes (MAMs) and CaActa pharmacologica Sinica · 2025Review
- Article
- Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury.Journal of translational medicine · 2025Review
- Hyperbaric Oxygen Upregulates Mst1 to Activate Keap1/Nrf2/HO-1 Pathway Resisting Oxidative Stress in a Rat Model of Acute Myocardial Infarction.Molecular biotechnology · 2025Article
- Mitophagy mediated by HIF-1α/FUNDC1 signaling in tubular cells protects against renal ischemia/reperfusion injury.Renal failure · 2024Article
- Mitochondria-Associated Organelle Crosstalk in Myocardial Ischemia/Reperfusion Injury.Journal of cardiovascular translational research · 2024Review
- Calcium signaling from sarcoplasmic reticulum and mitochondria contact sites in acute myocardial infarction.Journal of translational medicine · 2024Review
- Circular RNAs: a small piece in the heart failure puzzle.Functional & integrative genomics · 2024Review
- The Mst1/2-BNIP3 axis is required for mitophagy induction and neuronal viability under mitochondrial stress.Experimental & molecular medicine · 2024Article
- Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice.Scientific reports · 2024Article
- The structure and function of FUN14 domain-containing protein 1 and its contribution to cardioprotection by mediating mitophagy.Frontiers in pharmacology · 2024Review
- Mitophagy for cardioprotection.Basic research in cardiology · 2023Review
- Review
11 more citing papers are in PubMed but not listed here.
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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
Cardiac ischemia-reperfusion (I/R) injury results mainly from mitochondrial dysfunction and cardiomyocyte death. Mitophagy sustains mitochondrial function and exerts a pro-survival effect on the reperfused heart tissue. Mammalian STE20-like kinase 1 (Mst1) regulates chronic cardiac metabolic damage and autophagic activity, but its role in acute cardiac I/R injury, especially its effect on mitophagy, is unknown. The aim of this study is to explore whether Mst1 is involved in reperfusion-mediated cardiomyocyte death via modulation of FUN14 domain containing 1 (FUNDC1)-related mitophagy. Our data indicated that Mst1 was markedly increased in reperfused hearts. However, genetic ablation of Mst1 in Mst1-knockout (Mst1-KO) mice significantly reduced the expansion of the cardiac infarction area, maintained myocardial function and abolished I/R-mediated cardiomyocyte death. At the molecular level, upregulation of Mst1 promoted ROS production, reduced mitochondrial membrane potential, facilitated the leakage of mitochondrial pro-apoptotic factors into the nucleus, and activated the caspase-9-related apoptotic pathway in reperfused cardiomyocytes. Mechanistically, Mst1 activation repressed FUNDC1 expression and consequently inhibited mitophagy. However, deletion of Mst1 was able to reverse FUNDC1 expression and thus re-activate protective mitophagy, effectively sustaining mitochondrial homeostasis and blocking mitochondrial apoptosis in reperfused cardiomyocytes. Finally, we demonstrated that Mst1 regulated FUNDC1 expression via the MAPK/ERK-CREB pathway. Inhibition of the MAPK/ERK-CREB pathway prevented FUNDC1 activation caused by Mst1 deletion. Altogether, our data confirm that Mst1 deficiency sends a pro-survival signal for the reperfused heart by reversing FUNDC1-related mitophagy and thus reducing cardiomyocyte mitochondrial apoptosis, which identifies Mst1 as a novel regulator for cardiac reperfusion injury via modulation of mitochondrial homeostasis.
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