{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T14:09:45Z","timestamp":1764598185497,"version":"3.46.0"},"reference-count":46,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2025,7,29]],"date-time":"2025-07-29T00:00:00Z","timestamp":1753747200000},"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":["Liver International"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Non\u2010alcoholic fatty liver disease is now a significant public health issue globally. Salusin\u2010\u03b2, a vasoactive peptide, plays a role in lipid metabolism regulation, but its mechanism remains unreported.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We studied the effects of Salusin\u2010\u03b2 on lipid metabolism and its mechanism by creating a NAFLD model in C57BL\/6J mice and inducing steatosis in HepG2 cells. Then, shSalusin\u2010\u03b2 lentivirus was applied to transfect into the animals and cells, and the degree of lipid accumulation was assessed by staining and various biochemical indexes. Subsequently, Semi\u2010Quantitative PCR, Western Blot, molecular docking, and Co\u2010Immunoprecipitation were utilised to probe the downstream target FTO and then to verify the protein and mRNA changes of liposynthesis and catabolism genes downstream of FTO. Overexpressed FTO lentivirus was further employed to confirm this mechanism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The results showed that knockdown of Salusin\u2010\u03b2 significantly attenuated the degree of lipid accumulation in mice and cells. In addition, shSalusin\u2010\u03b2 inhibited the expression of FTO, thereby inhibiting the expression of downstream sterol regulatory element binding protein\u20101c, fatty acid synthase, and promoting the expression of peroxisome proliferators\u2010activated receptors \u03b1 and carnitine palmitoyl transferase 1. Transfection of overexpressed FTO then eliminated the regulatory effect of shSalusin\u2010\u03b2 on downstream molecules.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In conclusion, knockdown of Salusin\u2010\u03b2 reduced FTO production, thereby alleviating lipid metabolism disorders. This provides a potential mechanism for elucidating the reduction of lipid metabolism by knockdown of Salusin\u2010\u03b2 and a potential target for the treatment of NAFLD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/liv.70252","type":"journal-article","created":{"date-parts":[[2025,7,29]],"date-time":"2025-07-29T17:19:09Z","timestamp":1753809549000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Knockdown of Salusin\u2010\u03b2 Downregulates\n                    <scp>FTO<\/scp>\n                    to Inhibit Lipid Synthesis and Promote Lipolysis to Attenuate\n                    <scp>NAFLD<\/scp>"],"prefix":"10.1111","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-5959-1590","authenticated-orcid":false,"given":"Jintong","family":"Pan","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"},{"name":"Department of Medical Laboratory, The Central Hospital of Wuhan, Tongji Medical College Huazhong University of Science and Technology  Wuhan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinmeng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Chinese Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"},{"name":"Department of Spleen and Gastroenterology Hubei Provincial Hospital of Traditional Chinese Medicine, Hubei University of Chinese Medicine  Wuhan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ye","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zaohong","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuxue","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"},{"name":"Hubei Shizhen Laboratory Hubei University of Chinese Medicine  Wuhan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiang","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine Hubei University of Chinese Medicine  Wuhan Hubei China"},{"name":"Hubei Shizhen Laboratory Hubei University of Chinese Medicine  Wuhan Hubei 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