ArticleNutrition & diabetes2022
MST1 deletion protects β-cells in a mouse model of diabetes.
Article in Nutrition & diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Activation of MST1 protects filtration barrier integrity of diabetic kidney disease in mice through restoring the tight junctions of glomerular endothelial cells.Acta pharmacologica Sinica · 2025Article
- Terazosin, a repurposed GPR119 agonist, ameliorates mitophagy and β-cell function in NAFPD by inhibiting MST1-Foxo3a signalling pathway.Cell proliferation · 2025Article
- Neu-P11 Improves Type 2 Diabetes Mellitus Immune Function by Inhibiting the Hippo Signaling Pathway.International journal of endocrinology · 2025Article
- Hippo signaling pathway in polycystic ovary syndrome.Frontiers in endocrinology · 2025Review
- Association of MST1 in the First Trimester of Pregnancy with Gestational Diabetes Mellitus and Adverse Pregnancy Outcomes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
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Abstract
The pro-apoptotic kinase Mammalian Sterile 20-like kinase 1 (MST1), an integral component of the Hippo pathway, is a key regulator of organ size, stress response, and tissue homeostasis; its aberrant hyperactivation is linked to multiple pathological disorders including diabetes. Here we show that MST1 deletion in mice resulted in improved glucose tolerance and insulin secretion, and restored pancreatic β-cell mass as a result of improved β-cell survival and proliferation in the combined high fat/high sucrose and streptozotocin (HFS/STZ) model of β-cell destruction and diabetes. Importantly, the glucose-lowering effects in the MST1-knockout (KO) mice could be accounted to the enhanced β-cell mass and improved insulin secretion without changes in insulin sensitivity. Metabolic and morphological data suggest that normalization of blood glucose and insulin secretion, islet architecture, and β-cell mass by MST1 deletion in response to diabetes-induced injury occurs as a result of improved β-cell survival and proliferation establishing MST1 as potent regulator of physiological β-cell turnover.
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Registered trials
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