{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T12:14:46Z","timestamp":1790252086021,"version":"4.1.0"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","license":[{"start":{"date-parts":[[2025,3,28]],"date-time":"2025-03-28T00:00:00Z","timestamp":1743120000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2025,8]]},"abstract":"\n Key Points<\/jats:title>\n \n \n \n Activin A is implicated in profibrotic and prosenescent kidney injury and correlates with kidney injury markers in animals and humans.<\/jats:p>\n <\/jats:list-item>\n \n Follistatin, through activin A antagonism, reduces senescence burden, macrophage infiltration, and proinflammatory pathway activation in murine diabetic kidney disease.<\/jats:p>\n <\/jats:list-item>\n \n Follistatin and other antagonists of activin A signaling pathways may be promising, novel therapeutics for diabetic kidney disease.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n Circulating activin A, an inflammatory mediator implicated in profibrotic kidney injury and cellular senescence-induced adipose tissue dysfunction, is increased in human diabetic kidney disease (DKD) and directly correlates with kidney dysfunction. We tested the hypothesis that activin A increases kidney injury, senescent cell abundance, and macrophage infiltration in DKD and antagonism through follistatin (FS) therapy diminishes these effects.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n An accelerated nephropathy type 2 diabetes (db\/db) mouse model was generated by implantation of angiotensin II-loaded osmotic minipumps resulting in increased albuminuria and glomerular and tubular injury. Kidney repair effects of FS (5\n \u00b5<\/jats:italic>\n g intraperitoneal; two doses) were assessed through markers of kidney injury, fibrosis, inflammation, cellular senescence, and macrophage infiltration.\n In vitro<\/jats:italic>\n studies examined antiactivin effects of FS on high glucose-exposed human monocytes, renal fibroblasts, and renal tubule epithelial cells.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Activin A antagonism with FS reduced senescence (p19), proinflammatory (including senescence-associated secretory phenotype), and profibrotic markers including activin A. FS improved kidney morphology, restored podocyte markers (nephrin and Wilms tumor-1), and reduced kidney injury biomarkers, albuminuria and kidney fibrosis. FS decreased kidney macrophage and leukocyte infiltration and absent in melanoma 2 inflammasome activation. FS seemed to suppress inflammation through the toll-like receptor-4\/NF kappa-light-chain-enhancer of activated B cells pathway\n in vivo<\/jats:italic>\n further supported in human macrophages\n in vitro<\/jats:italic>\n . In addition, FS reduced hyperglycemia-induced renal fibroblast activation and renal tubule epithelial cell senescence\n in vitro<\/jats:italic>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Activin A is a mediator of kidney injury through macrophage-associated inflammation in murine DKD. FS acts through senomorphic activities which inhibit profibrotic, proinflammatory, and prosenescence signaling by activin A. Hence, antiactivin targeting may aid in the development of a promising, novel therapeutic for DKD.<\/jats:p>\n <\/jats:sec>","DOI":"10.34067\/kid.0000000776","type":"journal-article","created":{"date-parts":[[2025,3,30]],"date-time":"2025-03-30T16:19:18Z","timestamp":1743351558000},"page":"1278-1291","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":14,"title":["Activin A Antagonism with Follistatin Reduces Kidney Fibrosis, Injury, and Cellular Senescence-Associated Inflammation in Murine Diabetic Kidney Disease"],"prefix":"10.34067","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-1952-0141","authenticated-orcid":false,"given":"Xiaohui","family":"Bian","sequence":"first","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"},{"name":"Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-6407-3390","authenticated-orcid":false,"given":"Zachary K.","family":"Snow","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9099-172X","authenticated-orcid":false,"given":"Caroline J.","family":"Zinn","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-0829-0187","authenticated-orcid":false,"given":"Cody C.","family":"Gowan","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabena M.","family":"Conley","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9263-0891","authenticated-orcid":false,"given":"Anastasia L.","family":"Bratulin","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2230-2160","authenticated-orcid":false,"given":"Khaled M.","family":"Elhusseiny","sequence":"additional","affiliation":[{"name":"Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Jacksonville, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9868-4097","authenticated-orcid":false,"given":"Jordan","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Surgery, Mayo Clinic, Rochester, Minnesota"},{"name":"Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamar","family":"Tchkonia","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Center for Advanced Gerotherapeutics, Cedars-Sinai Medical Center, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1676-4905","authenticated-orcid":false,"given":"James L.","family":"Kirkland","sequence":"additional","affiliation":[{"name":"Division of Endocrinology and Metabolism, Department of Medicine, Center for Advanced 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