ArticleMolecular medicine (Cambridge, Mass.)2021
Elevated MST1 leads to apoptosis via depletion of YAP1 in cardiomyocytes exposed to high glucose.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 22 citations in OpenAlex.
- Assessment of dispersion metrics for estimating single-cell transcriptional variability.PLoS computational biology · 2026Article
- Inhibition of BRD4 sensitizes NSCLC cells to osimertinib by suppressing APT1 and promoting MST1 palmitoylation.Cell death discovery · 2025Article
- Hippo signaling pathway in human testis and seminoma: anticancer effect of verteporfin on human seminoma TCam-2 cells.Journal of molecular histology · 2025Article
- Insight into the cardioprotective effects of melatonin: shining a spotlight on intercellular Sirt signaling communication.Molecular and cellular biochemistry · 2025Review
- The Hippo Pathway in Breast Cancer: The Extracellular Matrix and Hypoxia.International journal of molecular sciences · 2024Review
- Tudor-SN promotes cardiomyocyte proliferation and neonatal heart regeneration through regulating the phosphorylation of YAP.Cell communication and signaling : CCS · 2024Article
- Effects of gas signaling molecule SOThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Research Progress of Maternal Metabolism on Cardiac Development and Function in Offspring.Nutrients · 2023Review
- Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease.International journal of molecular sciences · 2022Review
- The Hippo-YAP pathway in various cardiovascular diseases: Focusing on the inflammatory response.Frontiers in immunology · 2022Review
- Role of MiR-27a-3p in Intervertebral Disc Degeneration through Targeting RASSF5 via MST1/LATS1 and RAS/RAC1 Signaling Pathway.Journal of healthcare engineering · 2022Article
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7 authors at 2 institutions in 2 countries.
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Abstract
backgroundGestational diabetes mellitus is a risk factor for congenital heart defects. The article aimed to investigate the expression and roles of MST1, YAP1, Last1/2 and Survivin in modulating HG-induced cardiomyocyte apoptosis and maternal diabetes-induced heart abnormality.
methodsDiabetes mellitus was induced in rats using streptozotocin. The protein expression and phosphorylation analysis in fetal heart tissue was assessed by western blot and immunohistochemical staining. Hoechst 33342 staining assay was performed to explore H9C2 apoptosis. The gene and protein expression in H9C2 cells was assessed by quantitative PCR and western blot. Knockdown of gene expression was assessed by RNA interference.
resultsOur results revealed that increased MST1 protein levels in the heart tissues of the offspring of diabetic rats in vivo and in H9C2 cardiomyocytes under HG treatment in vitro, respectively. Knockdown and overexpression experiments showed that MST1 played a key role in mediating HG-induced apoptosis in cardiomyocytes. Downregulation of YAP1 was associated with HG-induced, MST1-mediated cardiomyocyte apoptosis. Further study showed that MST1 downregulated the protein level of YAP1 through mediation of YAP1 phosphorylation on Ser127 and Ser397; this process also required LATS1/2 participation. MST1 overexpression increased the phosphorylation levels of LATS1/2, which were also shown to be increased in the heart tissues of diabetic offspring. We also found that YAP1 mediated the expression of Survivin during HG-induced apoptosis, and the Survivin-inhibitor YM155 partially inhibited the role of YAP1 in suppressing apoptosis induced by HG in cardiomyocytes.
conclusionThese findings reveal a regulatory mechanism of MST1/YAP1/Survivin signaling in modulating cardiomyocyte apoptosis in vitro and maternal diabetes-induced congenital heart defects in vivo.
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