{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T06:01:29Z","timestamp":1789970489819,"version":"4.0.1"},"reference-count":38,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T00:00:00Z","timestamp":1789948800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:p>The structure and function of the centrosome and the adverse consequences of centrosome aberration are increasingly understood. Centrosome amplification (CA), probably the most studied form of centrosome abnormalities, occurs when a cell harbors more than two centrosomes. Diabetes is associated with the development of numerous diseases, the pathogenesis mechanisms of many of which, if not all, are not well understood. We have reported that diabetes triggers CA, which has pathological roles. In this context, we review the evidence that CA in diabetes promotes the development of diseases (e.g., cancer or vascular complications) via multiple mechanisms (e.g., genomic instability, inflammation, and aberrant ciliogenesis). CA is likely a mechanism underlying many, if not all, disease complications in diabetes.<\/jats:p>","DOI":"10.3389\/fcell.2026.1877870","type":"journal-article","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T05:35:08Z","timestamp":1789968908000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The roles of centrosome amplification in diabetes-associated diseases"],"prefix":"10.3389","volume":"14","author":[{"given":"Shao Chin","family":"Lee","sequence":"first","affiliation":[{"name":"Laboratory of Cell Biology, School of Life Sciences, Shanxi University","place":["Taiyuan, Shanxi, China"]},{"name":"Laboratory of Cell Biology, School of Life Sciences, Jiangsu Normal University","place":["Xuzhou, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng","family":"Xu","sequence":"additional","affiliation":[{"name":"Laboratory of Cell Biology, School of Life Sciences, Shanxi University","place":["Taiyuan, Shanxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi Gui","family":"Wu","sequence":"additional","affiliation":[{"name":"Laboratory of Cell Biology, School of Life Sciences, Shanxi University","place":["Taiyuan, Shanxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,21]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"409","DOI":"10.1016\/j.devcel.2018.10.026","article-title":"Oxidative stress in cells with extra centrosomes drives non-cell-autonomous invasion","volume":"47","author":"Arnandis","year":"2018","journal-title":"Dev. 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