{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T22:39:32Z","timestamp":1786747172370,"version":"build-2736575974"},"reference-count":69,"publisher":"Portland Press Ltd.","issue":"7","license":[{"start":{"date-parts":[[2020,3,30]],"date-time":"2020-03-30T00:00:00Z","timestamp":1585526400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,4,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Angiotensin II (Ang II) has been reported to aggravate hepatic fibrosis by inducing NADPH oxidase (NOX)-dependent oxidative stress. Alamandine (ALA) protects against fibrosis by counteracting Ang II via the MAS-related G-protein coupled (MrgD) receptor, though the effects of alamandine on hepatic fibrosis remain unknown. Autophagy activated by reactive oxygen species (ROS) is a novel mechanism of hepatic fibrosis. However, whether autophagy is involved in the regulation of Ang II-induced hepatic fibrosis still requires investigation. We explored the effect of alamandine on hepatic fibrosis via regulation of autophagy by redox balance modulation. In vivo, alamandine reduced CCl4-induced hepatic fibrosis, hydrogen peroxide (H2O2) content, protein levels of NOX4 and autophagy impairment. In vitro, Ang II treatment elevated NOX4 protein expression and ROS production along with up-regulation of the angiotensin converting enzyme (ACE)\/Ang II\/Ang II type 1 receptor (AT1R) axis. These changes resulted in the accumulation of impaired autophagosomes in hepatic stellate cells (HSCs). Treatment with NOX4 inhibitor VAS2870, ROS scavenger N-acetylcysteine (NAC), and NOX4 small interfering RNA (siRNA) inhibited Ang II-induced autophagy and collagen synthesis. Alamandine shifted the balance of renin\u2013angiotensin system (RAS) toward the angiotensin converting enzyme 2 (ACE2)\/alamandine\/MrgD axis, and inhibited both Ang II-induced ROS and autophagy activation, leading to attenuation of HSCs migration or collagen synthesis. In summary, alamandine attenuated liver fibrosis by regulating autophagy induced by NOX4-dependent ROS.<\/jats:p>","DOI":"10.1042\/cs20191235","type":"journal-article","created":{"date-parts":[[2020,3,30]],"date-time":"2020-03-30T10:27:53Z","timestamp":1585564073000},"page":"853-869","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Alamandine attenuates hepatic fibrosis by regulating autophagy induced by NOX4-dependent ROS"],"prefix":"10.1042","volume":"134","author":[{"given":"Yun","family":"Huang","sequence":"first","affiliation":[{"name":"Department of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China"},{"name":"Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China"},{"name":"State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral 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