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Here, we show that podocyte expression of decay-accelerating factor (DAF\/CD55), a complement C3 convertase regulator, crucially controls disease in murine models of adriamycin (ADR)-induced focal and segmental glomerulosclerosis (FSGS) and streptozotocin (STZ)-induced diabetic glomerulosclerosis. ADR induces enzymatic cleavage of DAF from podocyte surfaces, leading to complement activation. C3 deficiency or prevention of C3a receptor (C3aR) signaling abrogates disease despite DAF deficiency, confirming complement dependence. Mechanistic studies show that C3a\/C3aR ligations on podocytes initiate an autocrine IL-1\u03b2\/IL-1R1 signaling loop that reduces nephrin expression, causing actin cytoskeleton rearrangement. Uncoupling IL-1\u03b2\/IL-1R1 signaling prevents disease, providing a causal link. Glomeruli of patients with FSGS lack DAF and stain positive for C3d, and urinary C3a positively correlates with the degree of proteinuria. Together, our data indicate that the development and progression of glomerulosclerosis involve loss of podocyte DAF, triggering local, complement-dependent, IL-1\u03b2\u2013induced podocyte injury, potentially identifying new therapeutic targets.<\/jats:p>","DOI":"10.1084\/jem.20191699","type":"journal-article","created":{"date-parts":[[2020,7,27]],"date-time":"2020-07-27T13:16:46Z","timestamp":1595855806000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":79,"title":["Loss of decay-accelerating factor triggers podocyte injury and glomerulosclerosis"],"prefix":"10.1084","volume":"217","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6121-5326","authenticated-orcid":true,"given":"Andrea","family":"Angeletti","sequence":"first","affiliation":[{"name":"Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 1"},{"name":"Division of Nephrology, Dialysis, Transplantation, Giannina Gaslini Children's Hospital, Genoa, Italy 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiara","family":"Cantarelli","sequence":"additional","affiliation":[{"name":"Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 1"},{"name":"Dipartimento di Medicina e Chirurgia Universit\u00e0 di Parma, UO Nefrologia, Azienda Ospedaliera-Universitaria Parma, Parma, Italy 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Astgik","family":"Petrosyan","sequence":"additional","affiliation":[{"name":"GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Los Angeles, CA 4"},{"name":"Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, CA 5"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sofia","family":"Andrighetto","sequence":"additional","affiliation":[{"name":"Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 1"},{"name":"Renal Unit, Department of Medicine, University Hospital of Verona, Verona, Italy 6"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly","family":"Budge","sequence":"additional","affiliation":[{"name":"Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vivette D.","family":"D\u2019Agati","sequence":"additional","affiliation":[{"name":"Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 7"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4175-4602","authenticated-orcid":true,"given":"Susan","family":"Hartzell","sequence":"additional","affiliation":[{"name":"Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah","family":"Malvi","sequence":"additional","affiliation":[{"name":"\u201dF. 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