ArticleMedicine2025
The role of angiotensin (1-7) in pancreatic β-cell function and survival: A focus on autophagy.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
The angiotensin-converting enzyme 2/angiotensin (1-7) [Ang (1-7)]/Mas axis is recognized for its beneficial impact on pancreatic β-cell function and survival. However, the precise mechanisms underlying these benefits remain incompletely elucidated. This study aimed to elucidate the role of Ang (1-7) in pancreatic β-cells and determine whether autophagy is a critical factor in this mechanism. MIN6 cells were treated with palmitate and subjected to interventions including Ang (1-7), A779, and autophagy inhibitors. Cell viability was measured using the CCK-8 assay, and reactive oxygen species levels were quantified. Protein expression related to endoplasmic reticulum (ER) stress and autophagy was evaluated by western blotting. Apoptosis was analyzed using flow cytometry. Ang (1-7) reduced the expression of cleaved caspase-3 and P62, while increasing the expression of Beclin-1 in islets. Furthermore, palmitate treatment significantly elevated reactive oxygen species levels and upregulated the expression of ER stress markers such as GRP78, CHOP, ATF4, PERK, and p-eIF2α. Importantly, Ang (1-7) effectively mitigated these responses. Functionally, Ang (1-7) enhanced the viability and reduced the apoptotic rate of MIN6 cells exposed to palmitate. Mechanistically, Ang (1-7) alleviated ER stress, restored autophagic flux, and stimulated autophagy, as evidenced by increased expression of LC3-II and Beclin-1, and reduced p62 accumulation. These findings underscore that Ang (1-7) promotes the survival of MIN6 cells by restoring autophagic flux and enhancing autophagy.
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