{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T03:47:22Z","timestamp":1791604042637,"version":"4.3.4"},"reference-count":44,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"27","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2022,7,8]]},"abstract":"<jats:p>\n            Progerin, a product of\n            <jats:italic>LMNA<\/jats:italic>\n            mutation, leads to multiple nuclear abnormalities in patients with Hutchinson-Gilford progeria syndrome (HGPS), a devastating premature aging disorder. Progerin also accumulates during physiological aging. Here, we demonstrate that impaired insulin-like growth factor 1 receptor (IGF-1R)\/Akt signaling pathway results in severe growth retardation and premature aging in\n            <jats:italic>Zmpste24<\/jats:italic>\n            <jats:sup>\u2212\/\u2212<\/jats:sup>\n            mice, a mouse model of progeria. Mechanistically, progerin mislocalizes outside of the nucleus, interacts with the IGF-1R, and down-regulates its expression, leading to inhibited mitochondrial respiration, retarded cell growth, and accelerated cellular senescence. Pharmacological treatment with the PTEN (phosphatase and tensin homolog deleted on chromosome 10) inhibitor bpV (HOpic) increases Akt activity and improves multiple abnormalities in Zmpste24-deficient mice. These findings provide previously unidentified insights into the role of progerin in regulating the IGF-1R\/Akt signaling in HGPS and might be useful for treating\n            <jats:italic>LMNA<\/jats:italic>\n            -associated progeroid disorders.\n          <\/jats:p>","DOI":"10.1126\/sciadv.abo0322","type":"journal-article","created":{"date-parts":[[2022,7,8]],"date-time":"2022-07-08T17:59:05Z","timestamp":1657303145000},"source":"Crossref","is-referenced-by-count":30,"title":["Progerin modulates the IGF-1R\/Akt signaling involved in aging"],"prefix":"10.1126","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1261-7705","authenticated-orcid":true,"given":"Bo","family":"Jiang","sequence":"first","affiliation":[{"name":"College of Basic Medical Sciences, Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China."},{"name":"Institute of Health Sciences, China Medical University, Shenyang, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuan","family":"Wu","sequence":"additional","affiliation":[{"name":"College of Basic Medical Sciences, Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China."},{"name":"Institute of Health Sciences, China Medical University, Shenyang, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fang","family":"Meng","sequence":"additional","affiliation":[{"name":"College of Basic Medical Sciences, Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Limiao","family":"Si","sequence":"additional","affiliation":[{"name":"College of Basic Medical Sciences, Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, 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