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While ELP-004 minimally affected physiological RANKL-induced osteoclast maturation in murine bone marrow\u2013 and spleen-derived myeloid cells (BMSMCs) and human PBMC-derived cells, it potently interfered with osteoclast maturation driven by TNF\u03b1 or LTB4. The contribution of TRPC channels to osteoclastogenesis was examined using BMSMCs derived from TRPC4\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            or TRPC(1\u20137)\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, again revealing preferential interference with osteoclastogenesis driven by proinflammatory cytokines. ELP-004 also reduced bone erosion in a mouse model of rheumatoid arthritis. These investigations reveal TRPC channels as critical mediators of inflammatory bone erosion and provide insight into the major target of ELP-004, a drug currently in preclinical testing as a therapeutic for inflammatory arthritis.\n          <\/jats:p>","DOI":"10.1126\/sciadv.abm9843","type":"journal-article","created":{"date-parts":[[2025,1,15]],"date-time":"2025-01-15T19:00:44Z","timestamp":1736967644000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":4,"title":["Targeting TRPC channels for control of arthritis-induced bone erosion"],"prefix":"10.1126","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-9713-2307","authenticated-orcid":true,"given":"Suravi","family":"Ray","sequence":"first","affiliation":[{"name":"Fels Cancer Institute for Personalized Medicine, Department of Cancer &amp; Cellular Biology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5914-6336","authenticated-orcid":true,"given":"Jamie L.","family":"McCall","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology &amp; 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