{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T10:45:11Z","timestamp":1785840311102,"version":"3.56.0"},"reference-count":78,"publisher":"Ovid Technologies (Wolters Kluwer Health)","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Peripheral arterial disease affects &gt;200 million people worldwide and is characterized by impaired blood flow to the lower extremities. There are no effective medical treatments available. Using the mouse hind\u2010limb ischemia model and miRNA sequencing, we identified a novel miRNA, miR\u20106236, whose expression significantly elevated in ischemic mouse limbs compared with nonischemic limbs. The role of miR\u20106236 in general or in postischemic angiogenesis is not known. Here we describe its role using in\u00a0vivo and in\u00a0vitro models of peripheral arterial disease.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">In primary mouse and human endothelial cells, we studied the effect of simulated ischemia on miR\u20106236 expression and assessed its role in cell viability, apoptosis, migration, and tube formation during ischemia. Furthermore, we developed miR\u20106236 null mice and tested its role in postischemic perfusion recovery using the hind\u2010limb ischemia model. Lastly, using bioinformatics and gene expression analysis, we identified putative angiogenic miR\u20106236 targets. In\u00a0vitro simulated ischemia\u2010enhanced miR\u20106236 expression in mouse and human endothelial cells, whereas its inhibition improved viability, migration, tube formation, and reduced apoptosis. In\u00a0vivo ischemic mouse skeletal muscle tissue showed higher miR\u20106236 expression compared with nonischemic muscles. Loss of miR\u20106236 improved impaired postischemic perfusion recovery and poor angiogenesis associated with streptozotocin\u2010induced diabetes in mice. Six of the 8 miR\u20106236 predicted angiogenic target mRNAs showed expression consistent with regulation by miR\u20106236 in ischemic skeletal muscle.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">Our results show for the first time that miR\u20106236 plays a key role in regulating postischemic perfusion recovery and angiogenesis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.124.035923","type":"journal-article","created":{"date-parts":[[2024,11,28]],"date-time":"2024-11-28T03:33:51Z","timestamp":1732764831000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["miRNA\u20106236 Regulation of Postischemic Skeletal Muscle Angiogenesis"],"prefix":"10.1161","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8943-7406","authenticated-orcid":false,"given":"Arul 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