{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T03:10:38Z","timestamp":1784085038224,"version":"3.55.0"},"reference-count":31,"publisher":"The Endocrine Society","license":[{"start":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T00:00:00Z","timestamp":1782259200000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"National Science Foundation"},{"name":"Binational Science Foundation","award":["1613462"],"award-info":[{"award-number":["1613462"]}]},{"DOI":"10.13039\/501100003977","name":"Israel Science Foundation","doi-asserted-by":"publisher","award":["2295\/19"],"award-info":[{"award-number":["2295\/19"]}],"id":[{"id":"10.13039\/501100003977","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003977","name":"Israel Science Foundation","doi-asserted-by":"publisher","award":["3285\/24"],"award-info":[{"award-number":["3285\/24"]}],"id":[{"id":"10.13039\/501100003977","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Context<\/jats:title>\n                    <jats:p>Wolfram syndrome type 2 (WS2) is a rare monogenic diabetes syndrome caused by CISD2 mutations. Its cellular pathophysiology remains poorly understood, and no targeted therapies exist.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To characterize the clinical phenotype and cellular pathophysiology of the largest WS2 cohort to date, and to evaluate a novel, mechanistically targeted pharmacological intervention.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>Observational cohort study paired with ex vivo functional cellular assays and a proof-of-concept pilot clinical intervention.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Setting<\/jats:title>\n                    <jats:p>Multicenter academic and clinical institutions in Israel and the Palestinian territories.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Patients<\/jats:title>\n                    <jats:p>Twenty-two patients from 11 unrelated Palestinian families presenting with atypical juvenile-onset diabetes and gastrointestinal bleeding. Patient-derived fibroblasts (n = 4) were utilized for functional assays.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Intervention(s)<\/jats:title>\n                    <jats:p>Fibroblasts and 2 patients were treated with a combination of the iron chelator deferiprone (DFP) and the antioxidant N-acetylcysteine (NAC).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Main Outcome Measure(s)<\/jats:title>\n                    <jats:p>Clinical phenotype, CISD2 genetic analysis, mitochondrial labile iron (mLI) and reactive oxygen species (ROS) levels, organelle morphology, and preliminary clinical response (HbA1c, platelet aggregation).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Patients were homozygous for a CISD2 c.109G&amp;gt;C founder mutation (carrier rate 1:40). The clinical phenotype was expanded to include prevalent psychiatric morbidity and congenital heart defects. Patient fibroblasts exhibited profound mitochondrial and endoplasmic reticulum damage, with increased mLI (+25%, P &amp;lt; .0001) and mROS (+28%, P &amp;lt; .0001). In vitro DFP\u2013NAC treatment fully reversed these cellular anomalies. In a preliminary pilot study, 2 patients receiving DFP\u2013NAC demonstrated improved reported glycemic control and corrected platelet aggregation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>WS2 is an underdiagnosed monogenic diabetes driven by mitochondrial iron dysregulation and oxidative stress. Repurposing DFP\u2013NAC reverses this toxicity, offering a strong mechanistic rationale for future clinical trials.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1210\/clinem\/dgag250","type":"journal-article","created":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T11:43:47Z","timestamp":1782215027000},"source":"Crossref","is-referenced-by-count":1,"title":["Reversible mitochondrial iron toxicity in Wolfram syndrome type 2 monogenic diabetes"],"prefix":"10.1210","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-8452-2265","authenticated-orcid":false,"given":"Amitay","family":"Cohen","sequence":"first","affiliation":[{"name":"Division of Pediatric Endocrinology, Hadassah Hebrew University Medical Center , Jerusalem 91240 ,","place":["Israel"]},{"name":"Faculty of Medicine, The Hebrew University of Jerusalem , Jerusalem 91120 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