{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T03:16:52Z","timestamp":1790997412435,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2021,9,30]],"date-time":"2021-09-30T00:00:00Z","timestamp":1632960000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004772","name":"Natural Science Foundation of Ningxia Province","doi-asserted-by":"publisher","award":["2020AAC02021"],"award-info":[{"award-number":["2020AAC02021"]}],"id":[{"id":"10.13039\/501100004772","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004772","name":"Natural Science Foundation of Ningxia Province","doi-asserted-by":"publisher","award":["2020AAC02038"],"award-info":[{"award-number":["2020AAC02038"]}],"id":[{"id":"10.13039\/501100004772","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2021,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Atherosclerosis is a serious age\u2010related disease, which has a tremendous impact on health care globally. Macrophage inflammation is crucial for the initiation and progression of atherosclerosis, and microRNAs (miRNAs) recently have emerged as potent modulators of inflammation, while the underlying mechanisms of its involvement in homocysteine (Hcy)\u2010mediated macrophage inflammation of atherosclerosis remain largely unknown. Here, we demonstrated that elevated Hcy inhibits the expression of miR\u2010195\u20103p, which in turn enhances IL\u201031 expression and thereby causes the secretion of macrophages pro\u2010inflammatory factors IL\u20101\u03b2, IL\u20106 and TNF\u2010\u03b1 and accelerate atherosclerosis. Furthermore, we identified that Hcy can induce DNA hypermethylation and H3K9 deacetylation of miR\u2010195\u20103p promoter due to the increased the binding of DNMT3a and HDAC11 at its promoter. More importantly, Sp1 interacts with DNMT3a suppressed the binding of HDAC11 at miR\u2010195\u20103p promoter and promoted its transcription. In summary, our results revealed a novel mechanism that transcriptional and epigenetic regulation of miR\u2010195\u20103p inhibits macrophage inflammation through targeting IL\u201031, which provides a candidate diagnostic marker and novel therapeutic target in cardiovascular diseases induced by Hcy.<\/jats:p>","DOI":"10.1111\/acel.13485","type":"journal-article","created":{"date-parts":[[2021,9,30]],"date-time":"2021-09-30T19:20:23Z","timestamp":1633029623000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["miR\u2010195\u20103p alleviates homocysteine\u2010mediated atherosclerosis by targeting IL\u201031 through its epigenetics modifications"],"prefix":"10.1111","volume":"20","author":[{"given":"Jiantuan","family":"Xiong","sequence":"first","affiliation":[{"name":"School of Basic Medical Sciences Ningxia Medical University Yinchuan China"},{"name":"NHC Key Laboratory of Metabolic Cardiovascular Diseases Research 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