{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T16:10:57Z","timestamp":1747152657663,"version":"3.40.5"},"reference-count":27,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2024,10,27]],"date-time":"2024-10-27T00:00:00Z","timestamp":1729987200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"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"}]},{"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"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2025,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Patients with chronic kidney disease (CKD) frequently develop uremic cardiomyopathy, characterized by mitochondrial dysfunction as one of its pathologically significant mediators. Given that PM<jats:sub>2.5<\/jats:sub> specifically targets cardiac mitochondria, exacerbating toxicity, this study addresses the potential alterations in the severity of PM<jats:sub>2.5<\/jats:sub> toxicity in the context of CKD conditions. Female Wistar rats were exposed to PM<jats:sub>2.5<\/jats:sub> at a concentration of 250\u2009\u03bcg\/m<jats:sup>3<\/jats:sup> daily for 3\u2009h for 21\u2009days after which an adenine\u2010induced CKD model was developed. While both PM<jats:sub>2.5<\/jats:sub> exposure and the induction of CKD in rats lead to cardiomyopathy, the CKD animals exposed to PM<jats:sub>2.5<\/jats:sub> exhibited a notably severe extent of myocardial hypertrophy and fibrosis. ECG recordings in CKD+ PM<jats:sub>2.5<\/jats:sub> animals revealed a depressed ST segment and prolonged QRS interval, with both PM<jats:sub>2.5<\/jats:sub> and CKD animals displaying an elevated ST segment. Subcellular level analysis confirmed a significantly low mitochondrial copy number and a severe decline in mitochondrial bioenergetic function in the CKD+ PM<jats:sub>2.5<\/jats:sub> group. The prominent decline in PGC1\u2010\u03b1 further affirmed the severe mitochondrial functional deterioration in CKD+ PM<jats:sub>2.5<\/jats:sub> animals compared to other experimental groups. Additionally, myocardial calcification was enhanced in CKD+ PM<jats:sub>2.5<\/jats:sub> animals, heightening the susceptibility of CKD animals to PM<jats:sub>2.5<\/jats:sub> toxicity. In summary, our findings suggest that the increased vulnerability of CKD myocardium to PM<jats:sub>2.5<\/jats:sub>\u2010induced toxicity may be attributed to severe mitochondrial damage and increased calcification in the myocardium.<\/jats:p>","DOI":"10.1002\/tox.24437","type":"journal-article","created":{"date-parts":[[2024,10,28]],"date-time":"2024-10-28T05:19:42Z","timestamp":1730092782000},"page":"532-548","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Increased Susceptibility of Cardiac Tissue to <scp>PM<\/scp><sub>2.5<\/sub>\u2010Induced Toxicity in Uremic Cardiomyopathic Rats Is Linked to Elevated Levels of Mitochondrial Dysfunction"],"prefix":"10.1002","volume":"40","author":[{"given":"Bhavana","family":"Sivakumar","sequence":"first","affiliation":[{"name":"Vascular Biology Lab, School of Chemical and Biotechnology SASTRA Deemed University  Thanjavur Tamil Nadu 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