ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Mesencephalic Astrocyte-Derived Neurotrophic Factor Binds BAX to Preserve Mitochondrial Homeostasis and Energy Metabolism for Relieving Myocardial Hypertrophy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Neurotrophic Factors: Emerging Biology and Therapeutic Applications for Cardiovascular Diseases.Metabolites · 2026Review
- Demystifying anti-inflammatory therapeutic strategies against pancreatitis and concomitant diseases: a 2025 perspective.Theranostics · 2026Review
- Spatial transcriptomics analysis uncovers ER stress in MANF-deficient Purkinje cells underlying alcohol-induced cerebellar neurodegeneration in mice.Acta neuropathologica communications · 2025Article
- Mesencephalic Astrocyte-Derived Neurotrophic Factor Binds BAX to Preserve Mitochondrial Homeostasis and Energy Metabolism for Relieving Myocardial Hypertrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
Myocardial hypertrophy (MH) is a heart disease accompanied by mitochondrial energy disorder and oxidative stress for cardiomyocyte apoptosis. Mesencephalic astrocyte-derived neurotrophic factor (MANF), with anti-inflammation and cytoprotection, is found to be negatively correlated with atrial apoptosis and fibrillation. Here, the effect and mechanism of MANF on MH are studied. Myocardial cell-specific MANF knockout (MKO) mice are constructed to establish transverse aortic constriction (TAC) or angiotensin II (Ang II)-induced MH model. MANF is found to be upregulated by MH and protects cardiomyocytes against TAC or Ang II-induced MH. Mechanistically, through single-cell RNA sequencing and metabolomics analysis, MANF in cardiomyocytes is closely involved in glycolysis-oxidative phosphorylation balance and mitochondrial homeostasis. Furthermore, MANF interacts with pro-apoptotic BAX to inhibit BAX mitochondrial translocation, subsequently decreasing mitochondrial damage, cytochrome c release, and cardiomyocyte death. These results indicate a promising clinical value of MANF for MH treatment, and also preliminarily define MANF's role in mitochondrial energy production and mitochondria-associated apoptosis pathway.
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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 Socratic graph.