{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T18:59:11Z","timestamp":1790189951989,"version":"4.1.0"},"reference-count":33,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","license":[{"start":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:00:00Z","timestamp":1790812800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Atherosclerosis is driven by metabolic-immune crosstalk, in which trained immunity sustains vascular inflammation. MAP17 (membrane-associated protein 17), a redox- and metabolism-regulating adaptor protein, functions as a potential upstream driver of SGLT2 (sodium-glucose cotransporter 2). We aimed to determine whether MAP17 links hyperglycemia to glycolytic activation, inflammatory polarization, and plaque progression in atherosclerosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>MAP17 expression and its correlations with clinical risk factors were analyzed in serum from 30 patients with atherosclerosis. A trained immunity model was established in bone marrow\u2013derived macrophages via sustained high glucose and IFN-\u03b3 (interferon-\u03b3)\/lipopolysaccharide stimulation. Functional assays were performed after MAP17 overexpression\/knockdown, SGLT2 silencing, or glycolysis inhibition.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      MAP17 was significantly coupregulated in patients with atherosclerosis, with the highest levels observed in those with concomitant diabetes or metabolic syndrome, and closely associated with elevated proinflammatory M1-like cytokines. Immunohistochemistry of carotid plaques confirmed its colocalization with SGLT2 within CD68\n                      <jats:sup>+<\/jats:sup>\n                      macrophage-rich, lipid-laden, and inflamed regions. In bone marrow\u2013derived macrophages, high glucose robustly induced MAP17 expression, which unidirectionally upregulated SGLT2, enhanced glycolytic flux, increased lactate production, and promoted M1-like polarization and foam cell formation. MAP17 knockdown markedly suppressed SGLT2 expression, glycolysis, and TNF-\u03b1 (tumor necrosis factor-\u03b1)\/IL (interleukin)-1\u03b2 secretion, whereas MAP17 overexpression restored glycolytic activity, proinflammatory phenotype, and foam cell generation even in SGLT2-deficient cells. In diabetic chimeric\n                      <jats:italic toggle=\"yes\">Apoe<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      mice, MAP17 activation correlated with increased glycolytic marker expression, higher proinflammatory M1-like macrophage ratios, aggravated vascular inflammation, and greater plaque burden; these effects were mitigated by MAP17 or SGLT2 silencing, or by glycolysis inhibition.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>MAP17 is a key upstream controller of the SGLT2-glycolysis axis that promotes trained immunity and accelerates atherosclerosis. Targeting MAP17 may disrupt the metabolic-inflammatory feedback loop and represents a promising therapeutic strategy for diabetic atherosclerosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.324585","type":"journal-article","created":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T09:00:26Z","timestamp":1788426026000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["MAP17 Orchestrates SGLT2-Dependent Glycolytic Reprogramming to Drive Trained Immunity and Accelerate Atherosclerosis"],"prefix":"10.1161","volume":"46","author":[{"given":"Jianjin","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Vascular Surgery, First Affiliated Hospital of Dalian Medical University, China (L.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-4841-1338","authenticated-orcid":true,"given":"Fukang","family":"Zou","sequence":"additional","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fangbing","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guanyu","family":"Fang","sequence":"additional","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-5856-6858","authenticated-orcid":true,"given":"Kai","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4943-3451","authenticated-orcid":true,"given":"Haochen","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Stomatology (H.G.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7065-0605","authenticated-orcid":true,"given":"Kangkang","family":"Zhi","sequence":"additional","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6122-2569","authenticated-orcid":true,"given":"Lefeng","family":"Qu","sequence":"additional","affiliation":[{"name":"Department of Vascular and Endovascular Surgery (J.W., F.Z., F.L., G.F., K.C., K.Z., L.Q.), Second Affiliated Hospital of Naval Medical University, Shanghai, China."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-021-03392-8"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2005.09.068"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41392-022-00955-7"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41577-020-0285-6"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.chom.2017.02.003"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/978-3-030-28524-1_2"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2022.03.353"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehad787"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00130.2023"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1002\/advs.202100505"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.7150\/thno.62797"},{"key":"e_1_3_3_13_2","first-page":"1506","article-title":"A case report of fibromatosis originating from the right anterior scalene muscle.","volume":"38","author":"Okitsu H","year":"1990","unstructured":"Okitsu H, Tsuboi M, Nakajima S, Takahashi E, Hakoshima A, Ishimaru S. 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