{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T22:49:27Z","timestamp":1785192567248,"version":"3.55.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T00:00:00Z","timestamp":1633046400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Extracellular vesicles (EVs) have emerged as important mediators in cell\u2013cell communication; however, their relevance in pulmonary hypertension (PH) secondary to human immunodeficiency virus (HIV) infection is yet to be explored. Considering that circulating monocytes are the source of the increased number of perivascular macrophages surrounding the remodeled vessels in PH, this study aimed to identify the role of circulating small EVs and EVs released by HIV-infected human monocyte\u2013derived macrophages in the development of PH. We report significantly higher numbers of plasma-derived EVs carrying higher levels of TGF-\u03b21 (transforming growth factor-\u03b21) in HIV-positive individuals with PH compared with individuals without PH. Importantly, levels of these TGF-\u03b21\u2013loaded, plasma-derived EVs correlated with pulmonary arterial systolic pressures and CD4 counts but did not correlate with the Dl \u00a0CO or viral load. Correspondingly, enhanced TGF-\u03b21\u2013dependent pulmonary endothelial injury and smooth muscle hyperplasia were observed. HIV-1 infection of monocyte-derived macrophages in the presence of cocaine resulted in an increased number of TGF-\u03b21\u2013high EVs, and intravenous injection of these EVs in rats led to increased right ventricle systolic pressure accompanied by myocardial injury and increased levels of serum ET-1 (endothelin-1), TNF-\u03b1, and cardiac troponin-I. Conversely, pretreatment of rats with TGF-\u03b2 receptor 1 inhibitor prevented these EV-mediated changes. Findings define the ability of macrophage-derived small EVs to cause pulmonary vascular modeling and PH via modulation of TGF-\u03b2 signaling and suggest clinical implications of circulating TGF-\u03b2\u2013high EVs as a potential biomarker of HIV-associated PH.<\/jats:p>","DOI":"10.1165\/rcmb.2021-0010oc","type":"journal-article","created":{"date-parts":[[2021,5,20]],"date-time":"2021-05-20T13:53:58Z","timestamp":1621518838000},"page":"413-429","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":17,"title":["Extracellular Vesicle TGF-\u03b21 Is Linked to Cardiopulmonary Dysfunction in Human Immunodeficiency Virus"],"prefix":"10.1093","volume":"65","author":[{"given":"Balaji","family":"Krishnamachary","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, 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