{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T19:49:44Z","timestamp":1791575384203,"version":"4.3.4"},"reference-count":108,"publisher":"Ovid Technologies (Wolters Kluwer Health)","funder":[{"name":"Basic and Applied Basic Research Foundation of Guangdong Province","award":["2025A1515010471"],"award-info":[{"award-number":["2025A1515010471"]}]},{"name":"Basic and Applied Basic Research Foundation of Guangdong Province","award":["2023A1515012474"],"award-info":[{"award-number":["2023A1515012474"]}]},{"name":"Scientific and Technological Planning Project of Guangzhou City","award":["2023A03J0344"],"award-info":[{"award-number":["2023A03J0344"]}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["JASN"],"abstract":"<jats:p>Podocytes are key structural components of the glomerular filtration barrier and are essential for maintaining selective protein filtration. Podocyte dysfunction is closely associated with proteinuria and the progression of glomerulosclerosis, constituting the common pathological basis of various CKDs such as diabetic nephropathy and FSGS. While histone post-translational modifications (PTMs) have been extensively studied in podocyte biology, recent attention has shifted toward the regulatory roles of nonhistone PTMs. By modulating protein stability, activity, localization, and interactions, these modifications participate in core biological processes such as apoptosis, cytoskeletal remodeling, inflammatory signaling, and metabolic reprogramming. Nevertheless, the strength of evidence is not uniform across PTM categories. While some mechanisms have been directly demonstrated in podocytes, others are inferred mainly from broader kidney injury models or from studies in nonpodocyte cell types. Accordingly, not all reported PTM changes should be interpreted as equally well-established causal drivers of podocyte injury. This review focuses on the molecular regulatory networks and pathophysiological significance of major nonhistone PTMs, including acetylation, phosphorylation, methylation, lactylation, ubiquitination, and SUMOylation. We further propose a hypothesis-generating and integrative conceptual model of podocyte deterioration, linking initiating pathological stimuli to stress transduction and downstream effector decompensation that may culminate in structural collapse. Importantly, this proposed cascade is not intended to represent a universally validated linear sequence or a definitive disease mechanism. Rather, it provides an organizing framework to generate testable hypotheses. We further highlight the therapeutic promise of targeting nonhistone PTM pathways while acknowledging the considerable translational challenges that remain. By synthesizing the mechanistic landscape of nonhistone PTMs, this review provides an integrated framework for advancing our understanding of podocytopathy pathogenesis and fostering the development of precision-targeted therapies.<\/jats:p>","DOI":"10.1681\/asn.0000001242","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T17:01:25Z","timestamp":1786467685000},"update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Nonhistone Post-translational Modifications as Integrative Signaling Networks in Podocyte Injury and Glomerular Disease"],"prefix":"10.1681","author":[{"given":"Zhuoying","family":"He","sequence":"first","affiliation":[{"name":"Department of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanzhi","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-7432-8641","authenticated-orcid":false,"given":"Shaoguo","family":"Tao","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-1050-9509","authenticated-orcid":false,"given":"Yannic","family":"Becker","sequence":"additional","affiliation":[{"name":"Mount Desert Island Biological Laboratory, Bar Harbor, Maine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-0428-9763","authenticated-orcid":false,"given":"Patricia","family":"Schroder","sequence":"additional","affiliation":[{"name":"Mount Desert Island Biological Laboratory, Bar Harbor, Maine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Xiao","sequence":"additional","affiliation":[{"name":"Department of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-5740-838X","authenticated-orcid":false,"given":"Hermann","family":"Haller","sequence":"additional","affiliation":[{"name":"Mount Desert Island Biological Laboratory, Bar Harbor, 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