{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T04:35:52Z","timestamp":1792125352508,"version":"4.4.0"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:sec>\n            <jats:title>Background:<\/jats:title>\n            <jats:p>\n              Atherosclerosis is a chronic inflammatory disease, in which macrophages determine the progression of atherosclerotic plaques. However, no studies have investigated how METTL3 (methyltransferase like 3) in macrophages affects atherosclerotic plaque formation in vivo. Additionally, whether\n              <jats:italic>Braf<\/jats:italic>\n              mRNA is modified by METTL3-dependent N6-methyladenosine (m6A) methylation remains unknown.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods:<\/jats:title>\n            <jats:p>\n              We analyzed single-cell sequencing data of atherosclerotic plaques in mice fed with a high fat diet for different periods.\n              <jats:italic>\n                Mettl3\n                <jats:sup>fl\/fl<\/jats:sup>\n                Lyz\n              <\/jats:italic>\n              2\n              <jats:italic>\n                <jats:sup>cre<\/jats:sup>\n                Apoe\n                <jats:sup>\u2013\/\u2013<\/jats:sup>\n              <\/jats:italic>\n              mice and littermate control\n              <jats:italic>\n                Mettl3\n                <jats:sup>fl\/fl<\/jats:sup>\n                Apoe\n                <jats:sup>\u2013\/\u2013<\/jats:sup>\n              <\/jats:italic>\n              mice were generated and fed high fat diet for 14 weeks. In vitro, we stimulated peritoneal macrophages with ox-LDL (oxidized low-density lipoprotein) and tested the mRNA and protein expression levels of inflammatory factors and molecules regulating ERK (extracellular signal-regulated kinase) phosphorylation. To find METTL3 targets in macrophages, we performed m6A-methylated RNA immunoprecipitation sequencing and m6A-methylated RNA immunoprecipitation-qPCR. Further, point mutation experiments were used to explore m6A-methylated adenine. Using RNA immunoprecipitation assay, we explored m6A methylation-writing protein bound to\n              <jats:italic>Braf<\/jats:italic>\n              mRNA.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results:<\/jats:title>\n            <jats:p>\n              In vivo, METTL3 expression in macrophages increased with the progression of atherosclerosis. Myeloid cell\u2013specific METTL3 deletion negatively regulated atherosclerosis progression and the inflammatory response. In vitro, METTL3 knockdown or knockout in macrophages attenuated ox-LDL-mediated ERK phosphorylation rather than JNK (c-Jun N-terminal kinase) and p38 phosphorylation and reduced the level of inflammatory factors by affecting BRAF protein expression. The negative regulation of inflammation response caused by METTL3 knockout was rescued by overexpression of BRAF. In mechanism, METTL3 targeted adenine (39725126 in chromosome 6) on the\n              <jats:italic>Braf<\/jats:italic>\n              mRNA. Then, YTHDF1 could bind to m6A-methylated\n              <jats:italic>Braf<\/jats:italic>\n              mRNA and promoted its translation.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>\n              Myeloid cell\u2013specific\n              <jats:italic>Mettl3<\/jats:italic>\n              deficiency suppressed hyperlipidemia-induced atherosclerotic plaque formation and attenuated atherosclerotic inflammation. We identified\n              <jats:italic>Braf<\/jats:italic>\n              mRNA as a novel target of METTL3 in the activation of the ox-LDL-induced ERK pathway and inflammatory response in macrophages. METTL3 may represent a potential target for the treatment of atherosclerosis.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.122.318451","type":"journal-article","created":{"date-parts":[[2023,3,23]],"date-time":"2023-03-23T09:01:01Z","timestamp":1679562061000},"page":"755-773","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":75,"title":["METTL3 (Methyltransferase Like 3)-Dependent N6-Methyladenosine Modification on\n            <i>Braf<\/i>\n            mRNA Promotes Macrophage Inflammatory Response and Atherosclerosis in Mice"],"prefix":"10.1161","volume":"43","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6989-9494","authenticated-orcid":true,"given":"Qian","family":"Li","sequence":"first","affiliation":[{"name":"The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The 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