{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T20:01:09Z","timestamp":1790798469539,"version":"4.1.0"},"reference-count":64,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"13","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2026,9,29]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>\n                      Internal N7-methylguanosine (m\n                      <jats:sup>7<\/jats:sup>\n                      G) is a recently identified chemical modification of mammalian mRNA. Although the epitranscriptome plays a key role in regulating RNA metabolism and cellular function, the specific contribution of internal m\n                      <jats:sup>7<\/jats:sup>\n                      G to cardiovascular disease remains unknown. Atherosclerosis preferentially develops at sites of disturbed blood flow, which promotes endothelial activation; however, whether internal m\n                      <jats:sup>7<\/jats:sup>\n                      G regulates endothelial mechanotransduction and atherogenesis remains unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      We integrated epitranscriptomic profiling, human tissues, genetically modified mice, and targeted nanomedicine approaches to investigate the role of METTL7A (methyltransferase-like protein 7A), a putative internal m\n                      <jats:sup>7<\/jats:sup>\n                      G methyltransferase, in endothelial mechanobiology and atherosclerosis. Vascular endothelial cells were subjected to atheroprotective and atheroprone flow waveforms in vitro and in vivo. METTL7A function was assessed using RNA sequencing, liquid chromatography\u2013tandem mass spectrometry, crosslinking immunoprecipitation sequencing, RNA stability assays, and a clustered regularly interspaced short palindromic repeats (CRISPR)\/CRISPR-associated\u2013inspired RNA targeting system. METTL7A expression was examined in human coronary arteries with and without atherosclerosis. Atherosclerosis studies were conducted using global and endothelial-specific\n                      <jats:italic toggle=\"yes\">Mettl7a1<\/jats:italic>\n                      knockout mice. Endothelial METTL7A expression was restored using polymer-based nanoparticles delivering cadherin 5 (CDH5) promoter\u2013driven METTL7A plasmids or VCAM-1 (vascular cell adhesion molecule-1)\u2013targeted lipid nanoparticles delivering N1-methylpseudouridine\u2013modified METTL7A mRNA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Atheroprotective unidirectional flow significantly induced METTL7A expression, which promoted internal m\n                      <jats:sup>7<\/jats:sup>\n                      G methylation of endothelial transcripts without affecting cap-associated m\n                      <jats:sup>7<\/jats:sup>\n                      G. METTL7A preferentially bound AG-enriched motifs in protein-coding mRNAs and increased internal m\n                      <jats:sup>7<\/jats:sup>\n                      G methylation and stability of\n                      <jats:italic toggle=\"yes\">KLF4<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">NFKBIA<\/jats:italic>\n                      transcripts, thereby supporting vascular homeostasis. Endothelial METTL7A expression was significantly reduced by disturbed blood flow and in human atherosclerotic lesions. Global or endothelial-specific loss of\n                      <jats:italic toggle=\"yes\">Mettl7a1<\/jats:italic>\n                      exacerbated atherosclerosis in mice independent of serum lipid levels. Endothelial restoration of METTL7A through nanoparticle delivery of either a METTL7A plasmid or N1-methylpseudouridine\u2013modified METTL7A mRNA markedly attenuated atherosclerotic lesion formation in\n                      <jats:italic toggle=\"yes\">Mettl7a1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      <jats:italic toggle=\"yes\">\/<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      and\n                      <jats:italic toggle=\"yes\">ApoE<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      <jats:italic toggle=\"yes\">\/<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      METTL7A is a mechanosensitive internal m\n                      <jats:sup>7<\/jats:sup>\n                      G methyltransferase that maintains endothelial homeostasis by stabilizing the anti-inflammatory transcripts KLF4 (Kr\u00fcppel-like factor 4) and NFKBIA (NFKB inhibitor alpha). Loss of METTL7A disrupts endothelial function and accelerates atherogenesis. Endothelial restoration of METTL7A through complementary targeted nanoparticle platforms significantly reduces atherosclerotic burden. These findings uncover a novel epitranscriptomic mechanism governing vascular health and position METTL7A as a promising therapeutic target for atherosclerotic cardiovascular disease.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.125.075682","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T09:03:16Z","timestamp":1786438996000},"page":"1221-1237","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Mechanosensitive Endothelial METTL7A Regulates Internal m\n                    <sup>7<\/sup>\n                    G mRNA Methylation and Protects Against Atherosclerosis"],"prefix":"10.1161","volume":"154","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8688-8500","authenticated-orcid":true,"given":"Tzu-Pin","family":"Shentu","sequence":"first","affiliation":[{"name":"Department of Medicine (T.-P.S., Z.Z., J.L., C.-F.Y., J.Z., R.-T.H., B.A.M., B.X., J. 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