{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T20:43:14Z","timestamp":1790109794422,"version":"4.0.1"},"reference-count":99,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T00:00:00Z","timestamp":1785888000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    CD47-centered signaling, involving the functionally distinct CD47\u2013SIRP\u03b1 and TSP-1\u2013CD47 axes, has been increasingly implicated in the regulation of vascular inflammation, cellular clearance, and atherosclerotic plaque remodeling. This review examines these signaling pathways within two interrelated pathological dimensions: plaque formation and plaque vulnerability. During plaque formation, TSP-1\u2013CD47 signaling may contribute to endothelial dysfunction, leukocyte recruitment, vascular smooth muscle cell phenotypic modulation, and macrophage foam cell formation. In particular, atherosclerosis-specific experimental evidence supports a TSP-1\u2013CD47\u2013Nox1-dependent mechanism that promotes receptor-independent native low-density lipoprotein uptake through macrophage macropinocytosis. During plaque progression, the CD47\u2013SIRP\u03b1 axis functions primarily as an inhibitory phagocytic checkpoint. Engagement of macrophage SIRP\u03b1 recruits SHP-1\/2-dependent inhibitory signaling, suppresses cytoskeletal rearrangement, and impairs efferocytosis of apoptotic cells and lipid-rich cellular remnants, thereby contributing to secondary necrosis, necrotic core expansion, and persistent inflammation. In contrast, proposed effects of CD47-centered signaling on macrophage polarization, autophagy, and angiogenic responses are more context-dependent and are supported largely by indirect evidence derived from oncology, ischemic injury, wound-healing, metabolic disease, or\n                    <jats:italic>in vitro<\/jats:italic>\n                    models. To clarify these mechanistic boundaries, we classify the available evidence according to its source and directness, distinguishing atherosclerosis-specific findings from related vascular evidence and hypothesis-generating observations. Finally, we review current CD47-targeted therapeutic strategies and their translational limitations, including anemia, thrombocytopenia, off-target phagocytosis, uncertain effects on vascular repair, and the lack of cardiovascular clinical evidence. Although plaque-targeted delivery and cell-selective modulation may improve therapeutic specificity, the efficacy and long-term safety of CD47-targeted interventions in human atherosclerotic cardiovascular disease remain unproven. Finally, we address key translational bottlenecks\u2014including systemic hematological toxicities like anemia\u2014and discuss how plaque-specific biomimetic nano-delivery systems represent the mandatory path forward to safely realize the therapeutic potential of CD47-targeted interventions in clinical cardiology.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1850727","type":"journal-article","created":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T11:13:21Z","timestamp":1785928401000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["The CD47 signaling axis regulates the formation and vulnerability of atherosclerotic plaques: mechanism analysis and targeting strategies"],"prefix":"10.3389","volume":"17","author":[{"given":"Liyang","family":"Bai","sequence":"first","affiliation":[{"name":"Department of Neurology, The Neuroscience Center, The First Hospital of Jilin University, Jilin University","place":["Changchun, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baofeng","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Neurology, The Neuroscience Center, The First Hospital of Jilin University, Jilin University","place":["Changchun, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neurology, The Neuroscience Center, The First Hospital of Jilin University, Jilin University","place":["Changchun, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Neuroelectrophysiology, Zhongyi Northeast International Hospital","place":["Shenyang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lijuan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Neurology, The Neuroscience Center, The First Hospital of Jilin University, Jilin University","place":["Changchun, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Di","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Neurology, The Neuroscience Center, The First Hospital of Jilin University, Jilin University","place":["Changchun, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,5]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"973","DOI":"10.1016\/s1474-4422(24)00369-7","article-title":"Global, regional, and national burden of stroke and its risk factors, 1990-2021: a systematic analysis for the Global Burden of Disease Study 2021","volume":"23","year":"2024","journal-title":"Lancet Neurol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/s0140-6736(24)00757-8","article-title":"Global incidence, prevalence, years lived with disability (YLDs), 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