{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T01:16:21Z","timestamp":1783473381585,"version":"3.55.0"},"reference-count":27,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T00:00:00Z","timestamp":1779926400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T00:00:00Z","timestamp":1779926400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Nephrology"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>Peritoneal fibrosis (PF) is a progressive complication of long\u2010term peritoneal dialysis, driven primarily by high\u2010glucose\u2013induced mesothelial injury, epithelial\u2013mesenchymal transition, and chronic inflammation. Emerging evidence implicates autophagy dysfunction as a pivotal contributor to PF progression. Finerenone, a novel non\u2010steroidal mineralocorticoid receptor antagonist, has shown potent anti\u2010fibrotic and anti\u2010inflammatory effects in cardiorenal diseases, yet its role in peritoneal fibrosis remains incompletely understood. This study aimed to investigate whether Finerenone alleviates PF by regulating autophagy activity in peritoneal mesothelial cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A mouse model of peritoneal fibrosis was established by daily intraperitoneal injection of 4.25% glucose\u2010based peritoneal dialysis solution for 28\u2009days. Finerenone (10\u2009mg\/kg) was administered orally concomitantly with dialysis fluid for 28\u2009days. In\u00a0vitro, human peritoneal mesothelial cells (HPMCs) were stimulated with TGF\u2010\u03b21 (2\u2009ng\/mL, 36\u2009h) to induce fibrotic transformation. Cellular morphology, collagen deposition (Masson staining), and fibrosis markers (\u03b1\u2010SMA, Fibronectin, Collagen I, and E\u2010cadherin) were assessed by immunohistochemistry, immunofluorescence, and Western blot. Autophagy activity was evaluated by LC3\u2010II\/LC3\u2010I ratio, p62 degradation, Beclin\u20101 and Atg5 expression, and chloroquine (CQ) co\u2010treatment. Finally, Atg5 was silenced using siRNA to confirm its role in Finerenone\u2010induced autophagy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Finerenone markedly attenuated peritoneal thickening and collagen accumulation in\u00a0vivo and suppressed TGF\u2010\u03b21\u2010induced fibrotic phenotype in HPMCs. Finerenone decreased \u03b1\u2010SMA, Fibronectin, and Collagen I expression while restoring E\u2010cadherin levels. Mechanistically, Finerenone reversed TGF\u2010\u03b21\u2010induced autophagy blockade, as evidenced by increased LC3\u2010II\/LC3\u2010I and Beclin\u20101, upregulated Atg5, and decreased p62 accumulation, indicating enhanced autophagic flux. The autophagy inhibitor CQ abolished these protective effects, leading to LC3\u2010II and p62 accumulation. Moreover, Atg5 knockdown counteracted Finerenone\u2010mediated suppression of fibrosis\u2010related proteins, confirming that Finerenone's anti\u2010fibrotic effects depend on Atg5\u2010mediated autophagy activation. Finerenone also reduced pro\u2010inflammatory cytokines (TGF\u2010\u03b21, IL\u20106, and IL\u20101\u03b2), suggesting that autophagy restoration alleviates inflammation in parallel.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Finerenone alleviates peritoneal fibrosis, at least in part, by restoring Atg5\u2010mediated autophagic flux and suppressing inflammation in peritoneal mesothelial cells. These findings provide mechanistic insight into its antifibrotic effects and support autophagy modulation as a potential therapeutic strategy for peritoneal dialysis\u2013associated complications.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nep.70222","type":"journal-article","created":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T01:30:12Z","timestamp":1780018212000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Finerenone Attenuates Peritoneal Fibrosis by Restoring Autophagy Flux"],"prefix":"10.1111","volume":"31","author":[{"given":"Feng","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Nephrology, Taiyuan Central Hospital The Ninth Clinical Medical College of Shanxi Medical University  Taiyuan City Shanxi Province China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YaoRong","family":"Wang","sequence":"additional","affiliation":[{"name":"Department 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