{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T07:35:52Z","timestamp":1789630552311,"version":"build-2803163510"},"reference-count":25,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2025,1,28]],"date-time":"2025-01-28T00:00:00Z","timestamp":1738022400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001411","name":"Indian Council of Medical Research","doi-asserted-by":"publisher","award":["3\/1\/2(22)\/Env\/2021\u2010NCD\u2010II"],"award-info":[{"award-number":["3\/1\/2(22)\/Env\/2021\u2010NCD\u2010II"]}],"id":[{"id":"10.13039\/501100001411","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001409","name":"Department of Science and Technology, Ministry of Science and Technology, India","doi-asserted-by":"publisher","award":["CRG\/2021\/000227"],"award-info":[{"award-number":["CRG\/2021\/000227"]}],"id":[{"id":"10.13039\/501100001409","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>The cardiovascular risks linked to PM<jats:sub>2.5<\/jats:sub> include calcification in both vasculature and myocardial tissues, leading to structural changes and functional decline. Through the selection of a clinically proven endogenous agent, sodium thiosulfate (STS), capable of addressing PM<jats:sub>2.5<\/jats:sub> related cardiac abnormalities, we not only address the absence of effective solutions to mitigate PM<jats:sub>2.5<\/jats:sub> toxicity, but also provide evidence for the repurposing potential of STS in ameliorating PM<jats:sub>2.5<\/jats:sub> induced cardiac damage. Female Wistar rats were exposed to PM<jats:sub>2.5<\/jats:sub> (250\u2009\u03bcg\/m<jats:sup>3<\/jats:sup>) for 3\u2009h daily for 21\u2009days. STS was administered thrice weekly for 3\u2009weeks during exposure after which the hearts were excised and mounted on a Langendorff apparatus for induction of ischemia\u2013reperfusion injury (IR). STS administration improved cardiac function in PM<jats:sub>2.5<\/jats:sub> exposed rat hearts, accompanied by increased expression of the master regulator gene PGC1\u2010\u03b1 and increased mitochondrial mass. Moreover, STS restored bioenergetic function and balanced mitochondrial fission\u2013fusion dynamics. The beneficial effects of STS were further evidenced by its ability to scavenge metals, thereby reducing heavy metal deposition in mitochondria and alleviating oxidative stress and inflammation. Furthermore, STS facilitated the clearance of damaged mitochondria through mitophagy. Additionally, STS activated the PI3K\/AKT\/GSK3\u00df signaling pathway, providing cardio protection against IR injury in PM<jats:sub>2.5<\/jats:sub>\u2010exposed hearts by preserving mitochondrial function. These results underscore the potential therapeutic benefits of STS in mitigating the adverse cardiac effects induced by PM<jats:sub>2.5<\/jats:sub> exposure. The translation of these findings to clinical practice holds promise for the development of targeted interventions aimed at reducing the cardiovascular toxicity associated with PM<jats:sub>2.5<\/jats:sub> exposure.<\/jats:p>","DOI":"10.1002\/tox.24473","type":"journal-article","created":{"date-parts":[[2025,1,28]],"date-time":"2025-01-28T11:16:21Z","timestamp":1738062981000},"page":"912-923","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Mitigating <scp>PM<sub>2.5<\/sub><\/scp> Induced Myocardial Metal Deposition Through Sodium Thiosulfate Resulted in Reduction of Cardiotoxicity and Physiological Recovery From Ischemia\u2013Reperfusion via Mitochondrial Preservation"],"prefix":"10.1002","volume":"40","author":[{"given":"Bhavana","family":"Sivakumar","sequence":"first","affiliation":[{"name":"Cardiovascular Center, College of Medicine University of Cincinnati  Cincinnati Ohio 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