{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T06:21:00Z","timestamp":1784614860447,"version":"3.55.0"},"reference-count":38,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2024,11,18]],"date-time":"2024-11-18T00:00:00Z","timestamp":1731888000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Phytotherapy Research"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Chronic kidney diseases (CKD) is a serious threat to people's health with renal fibrosis as the major pathological feature. The absent in melanoma 2 (AIM2) has recently been proposed to play a critical role in CKD. Emodin is a major bioactive compound from rhubarb, which is widely used for clinical treatment of renal disease. The aim of this study is to elucidate the effect of emodin on unilateral ureteral obstruction (UUO) model mice and its association with the AIM2 inflammasome. In this study, we established the UUO\u2010induced mice renal interstitial fibrosis in\u00a0vivo and bone marrow\u2010derived macrophages (BMDMs) model in\u00a0vitro. The BUN, SCr, TNF\u2010\u03b1, IL\u20101\u03b2 in serum were examined. The degree of renal damage and fibrosis were determined by histological assessment. Immunofluorescence, western blot, and Co\u2010IP were used to determine the mechanisms of emodin against CKD. Emodin could improve UUO\u2010induced abnormal renal function and histopathological abnormalities. It could also ameliorate renal fibrosis, evidenced by inhibiting the expression of \u03b1\u2010SMA, TGF\u2010\u03b21, FN, and collagen I. Mechanistically, emodin significantly suppressed AIM2 inflammasome as well as its components including ASC, cleaved caspase\u20101, and IL\u20101\u03b2 both in\u00a0vivo and in\u00a0vitro. Further studies demonstrated that emodin inhibited K27\u2010linked polyubiquitination of AIM2 by targeting on K64 sites of the lysine residues. In summary, emodin could hinder the activation of AIM2 inflammasome in UUO model mice through K27\u2010linked polyubiquitination to reduce renal fibrosis. Emodin is a possible therapeutic option for CKD treatment.<\/jats:p>","DOI":"10.1002\/ptr.8390","type":"journal-article","created":{"date-parts":[[2024,11,19]],"date-time":"2024-11-19T01:14:44Z","timestamp":1731978884000},"page":"551-563","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Emodin Inhibits\n                    <scp>AIM2<\/scp>\n                    Inflammasome Activation via Modulating\n                    <scp>K27<\/scp>\n                    \u2010Linked Polyubiquitination to Attenuate Renal Fibrosis"],"prefix":"10.1002","volume":"39","author":[{"given":"Lidan","family":"Lu","sequence":"first","affiliation":[{"name":"Department of Gynaecology Changshu Hospital Affiliated to Nanjing University of Chinese Medicine  Changshu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruonan","family":"Shuang","sequence":"additional","affiliation":[{"name":"School of Integrated Chinese and 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