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Preliminary data showed that, with a five-fold increase, miR-26b was highly expressed in human atherosclerotic plaques compared to healthy vessels. Therefore, we aimed to determine its cell-specific effects on atherosclerosis development and its therapeutic potential.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>We examined the role of miR-26b in atherosclerosis by using whole-body Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 and myeloid cell-specific miR-26b-deficient (LysM-Cre) mice on a Western-type diet (WTD). Atherosclerotic plaque size and phenotype, as well as the phenotype and function of bone marrow-derived macrophages (BMDMs) from Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 mice, were investigated. Lipid nanoparticles (LNPs) served as vehicles for miR-26b mimics to restore miR-26b levels in miR-26b-deficient BMDMs in vitro and in mice in vivo.<\/jats:p>\n                    <jats:p>Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 mice have a striking 2.8-fold increase in atherosclerotic lesion size in the aortic arch after 12-week WTD, compared to control Apoe\u2212\/\u2212, while lesions in the aortic root were unaffected. Consistent with a more advanced plaque phenotype, collagen, smooth muscle cell, and necrotic core content were all significantly increased in plaques from Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 mice, whilst the relative macrophage content was significantly reduced. This phenotype could also be observed in Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 mice after 4-week WTD. Intriguingly, relative plaque size in the arches of Apoe\u2212\/\u2212LysmCre+Mir26bfl\/fl mice was increased by 2.5-fold, suggesting a role for myeloid-specific miR-26b in atherosclerosis development. Further highlighting its myeloid-specific effects, Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 BMDMs showed an increase in pro-inflammatory cytokine secretion, which could be rescued by LNPs containing miR-26b mimics. MiR-26b pull-down analysis revealed AnnexinA2 as one of the novel targets playing a key role in these effects, which could be validated in BMDMs in vitro. Furthermore, in vivo treatment of Apoe\u2212\/\u2212Mir26b\u2212\/\u2212 mice as well as ex vivo treatment of human plaques with miR-26b-mimic-loaded LNPs demonstrated their therapeutic potential and human relevance, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Overall, our results clearly demonstrate an atheroprotective role of miR-26b by attenuating lesion formation, mainly by suppressing inflammation and stimulating collagen breakdown. Furthermore, the therapeutic potential of miR-26b mimic-loaded LNPs could be proven, opening up new avenues for miRNA-based treatment options in the future.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvaf234","type":"journal-article","created":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T12:58:42Z","timestamp":1762865922000},"page":"2700-2713","source":"Crossref","is-referenced-by-count":8,"title":["<i>MicroRNA-26b\u2212\/\u2212<\/i>\n                    augments atherosclerosis, while mimic-loaded nanoparticles reduce atherogenesis"],"prefix":"10.1093","volume":"121","author":[{"given":"Linsey J F","family":"Peters","sequence":"first","affiliation":[{"name":"Institute for Cardiovascular Prevention (IPEK), LMU Munich , 80336 Munich ,","place":["Germany"]},{"name":"Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University , 52074 Aachen 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Diseases (Medical Clinic II), RWTH Aachen , 52074 Aachen ,","place":["Germany"]},{"name":"BHF Centre for Cardiovascular Sciences, University of Edinburgh , Edinburgh ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4906-0384","authenticated-orcid":false,"given":"Marion J","family":"Gijbels","sequence":"additional","affiliation":[{"name":"Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University , Maastricht 6229 ER ,","place":["The Netherlands"]},{"name":"Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences: Atherosclerosis & Ischemic Syndrome; Amsterdam Infection and Immunity: Inflammatory Diseases; Amsterdam UMC Location University of Amsterdam , Meibergdreef 9, Amsterdam ,","place":["The 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