ArticleCell & bioscience2022
FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- ASIV Attenuates Cisplatin-Induced Proximal Tubular Injury by Enhancing Mitochondrial Biogenesis and Mitophagy Through the ADRA1A/AMPK/FOXO3A Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- UA-30 ameliorates motor deficits through RalA-mediated mitophagy in ALS mice.The Journal of clinical investigation · 2026Article
- EGCG targeting autophagy in cardiovascular diseases: mechanisms and therapeutic potential.Molecular biology reports · 2026Review
- FGF21-FGFR1 signaling protects against cardiac hypertrophy by regulating PINK1-mediated mitophagy pathway.Journal of advanced research · 2026Article
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Overexpression of As3mt Attenuates Sodium Arsenite Induced Ferritinophagy and Hepatic Lipid Accumulation in Mice.Biological trace element research · 2026Article
- A zinc-coordinated cascade-responsive therapeutic nanoassembly for remodeling the pathological microenvironment and restoring mitochondrial homeostasis in spinal cord injury.Journal of nanobiotechnology · 2026Article
- Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026Review
- 4E-BP inhibition ameliorates heart failure through translational upregulation of SERCA2a and modulation of mitochondrial redox signaling in cardiomyocytes.Redox biology · 2026Article
- Brain age gap as biomarker linking cardiovascular diseases genetic susceptibility and causality.iScience · 2026Article
- Synaptotagmin-7 drives stress-induced cardiomyocyte necroptosis via the p53-Bak-mPTP axis.Theranostics · 2026Article
- Homocysteine promotes cardiomyocyte hypertrophy through inhibiting β-catenin/ FUNDC1 mediated mitophagy.Scientific reports · 2025Article
- Coordination of SLC39A1 and DRP1 facilitates HCC recurrence by impairing mitochondrial quality control.Clinical and translational medicine · 2025Article
- Enhanced SIRT3 expression restores mitochondrial quality control mechanism to reverse osteogenic impairment in type 2 diabetes mellitus.Bone research · 2025Article
- VEGFR3 mitigates hypertensive nephropathy by enhancing mitophagy via regulating crotonylation of HSPA1L.Cell communication and signaling : CCS · 2025Article
- Synaptotagmin-1 attenuates myocardial programmed necrosis and ischemia/reperfusion injury through the mitochondrial pathway.Cell death & disease · 2025Article
- Article
- Mitochondrial quality control in health and cardiovascular diseases.Frontiers in cell and developmental biology · 2023Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSustained cardiac hypertrophy often develops maladaptive myocardial remodeling, and eventually progresses to heart failure and sudden death. Therefore, maladaptive hypertrophy is considered as a critical therapeutic target for many heart diseases. Mitophagy, a crucial mechanism in mitochondria quality control and cellular homeostasis, has been implicated in diverse cardiac disorders such as myocardial infarction, diabetic cardiomyopathy, cardiac hypertrophy and heart failure. However, what role mitophagy plays in heart diseases remains an enigma. PARKIN functions as an E3 ubiquitin protein ligase and mediates mitophagy cascades. It is still unclear whether PARKIN participates in the regulation of cardiac hypertrophy.
resultsPARKIN was downregulated in cardiomyocytes and hearts under hypertrophic stress. Enforced expression of PARKIN inhibited Ang II-induced cardiomyocyte hypertrophy. Compared to wide-type mice with Ang II-induced cardiac hypertrophy, Parkin transgenic mice subjected to Ang II administration showed attenuated cardiac hypertrophy and improved cardiac function. In addition, mitophagy machinery was impaired in response to Ang II, which was rescued by overexpression of PARKIN. PARKIN exerted the anti-hypertrophy effect through restoring mitophagy. In further exploring the underlying mechanisms, we found that PARKIN was transcriptionally activated by FOXO3a. FOXO3a promoted mitophagy and suppressed cardiac hypertrophy by targeting Parkin.
conclusionsThe present study reveals a novel cardiac hypertrophy regulating model composed of FOXO3a, PARKIN and mitophagy program. Modulation of their levels may provide a new approach for preventing cardiac hypertrophy and heart failure.
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