ArticleWorld journal of gastroenterology2025
Lysine acetyltransferase 2A-mediated succinylation of adenosine monophosphate-activated protein kinase suppresses gallstone formation by inhibiting inflammation and pyroptosis.
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Succinylation: A novel regulatory axis in cholelithiasis-insights from lysine acetyltransferase 2A/adenosine monophosphate-activated protein kinase signaling.World journal of gastroenterology · 2026Article
- Potential of lysine succinylation as a therapeutic target for gallstone formation: An insightful strategy.World journal of gastroenterology · 2026Article
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9 authors.
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Abstract
backgroundCholelithiasis is a prevalent biliary tract disorder primarily characterized by gallbladder or biliary stone formation. Although succinylation has been extensively studied as a protein post-translational modification, its role in cholelithiasis remains unexplored.
aimTo investigate the functional role of succinylation in cholelithiasis and determine its underlying molecular mechanisms.
methodsA murine cholelithiasis model was established through high-fat diet feeding, followed by isolation of mouse gallbladder mucosal epithelial cells (GMECs) for
resultsOur findings demonstrated that lysine acetyltransferase 2A (KAT2A)-mediated succinylation regulated gallstone formation. KAT2A overexpression inhibited the pyroptosis, inflammatory responses, and promoted the activation of the adenosine monophosphate-activated protein kinase (AMPK)/silent information regulator 1 (SIRT1) signaling pathway in GMECs. Mechanistically, AMPK exhibited succinylation at lysine 170 (K170). Notably, AMPK inhibition significantly increased pyroptosis rates, inflammatory responses, and pyroptosis-related protein expression in GMECs. Furthermore,
conclusionKAT2A-mediated succinylation of AMPK inhibited cholelithiasis progression by modulating the AMPK/SIRT1 signaling pathway, offering potential therapeutic strategies for this condition.
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