{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T05:33:36Z","timestamp":1761802416150,"version":"build-2065373602"},"reference-count":52,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T00:00:00Z","timestamp":1761177600000},"content-version":"vor","delay-in-days":22,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Microcirculation"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We have previously demonstrated angiogenic impairment, inflammation, and endothelial vasomotor dysfunction in the visceral adipose vasculature of obese individuals. Here, we investigated the role of calcium\/calmodulin\u2010dependent protein kinase II (CaMKII) in the regulation of vascular phenotype in the adipose microvasculature.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Using visceral and subcutaneous fat specimens biopsied from obese subjects (BMI 48\u2009\u00b1\u20099\u2009kg\/m\n                      <jats:sup>2<\/jats:sup>\n                      , age 38\u2009\u00b1\u200911\u2009years), we examined the effect of CaMKII antagonism on acetylcholine\u2010mediated, endothelium\u2010dependent vasodilation of isolated arterioles using videomicroscopy and studied angiogenic capillary sprouting capacity ex\u00a0vivo.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pharmacological inhibition of CaMKII with KN\u201093 improved endothelium\u2010dependent vasodilation of isolated visceral arterioles by 3\u2010fold (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001 vs. control) and increased visceral fat sprouting capacity by 2.5\u2010fold (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). Inhibition of endothelial nitric oxide synthase with N(\u03c9)\u2010nitro\u2010l\u2010arginine methyl ester blunted KN\u201093\u2010induced improvements in vasodilation and angiogenesis, suggesting dependence on increased nitric oxide bioavailability. KN\u201093 had no effect on subcutaneous angiogenic capacity, which exhibited preserved angiogenic growth compared to visceral fat. KN\u201093 exposure was associated with reduced reactive oxygen species generation and decreased vascular gene expression of\n                      <jats:italic>JUN<\/jats:italic>\n                      ,\n                      <jats:italic>NFAT5<\/jats:italic>\n                      , and\n                      <jats:italic>CAMKII<\/jats:italic>\n                      signaling components.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings suggest that CaMKII signaling may negatively modulate microvascular function, contribute to increased oxidative stress, and pro\u2010inflammation observed in the visceral adipose microenvironment in obesity.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/micc.70033","type":"journal-article","created":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T07:12:16Z","timestamp":1761203536000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>CaMKII<\/scp>\n                    Antagonism Improves Vascular Dysfunction in the Visceral Adipose Microvasculature of Obese Subjects"],"prefix":"10.1111","volume":"32","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9143-4538","authenticated-orcid":false,"given":"Bulbul","family":"Ahmed","sequence":"first","affiliation":[{"name":"Evans Department of Medicine and Whitaker Cardiovascular Institute Boston University Chobanian &amp; Avedisian School of Medicine  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Melissa G.","family":"Farb","sequence":"additional","affiliation":[{"name":"Evans Department of Medicine and Whitaker Cardiovascular Institute Boston University Chobanian &amp; Avedisian School of Medicine  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sophia","family":"D'Alessandro","sequence":"additional","affiliation":[{"name":"Evans Department of Medicine and Whitaker Cardiovascular Institute Boston University Chobanian &amp; Avedisian School of Medicine  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luise","family":"Pernar","sequence":"additional","affiliation":[{"name":"Division of Weight Loss Surgery Boston Medical Center  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brain","family":"Carmine","sequence":"additional","affiliation":[{"name":"Division of Weight Loss Surgery Boston Medical Center  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donald T.","family":"Hess","sequence":"additional","affiliation":[{"name":"Division of Weight Loss Surgery Boston Medical Center  Boston Massachusetts USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kenneth","family":"Walsh","sequence":"additional","affiliation":[{"name":"Hematovascular Biology Center University of Virginia  Charlottesville Virginia USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noyan","family":"Gokce","sequence":"additional","affiliation":[{"name":"Evans Department of Medicine and Whitaker Cardiovascular Institute Boston University Chobanian &amp; 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