{"id":5405,"date":"2022-05-23T08:57:52","date_gmt":"2022-05-23T12:57:52","guid":{"rendered":"https:\/\/health.uconn.edu\/neuroscience\/?p=5405"},"modified":"2022-05-23T11:43:17","modified_gmt":"2022-05-23T15:43:17","slug":"activation-of-macrophage-trpm2-and-cd36-promotes-atherosclerosis","status":"publish","type":"post","link":"https:\/\/health.uconn.edu\/neuroscience\/2022\/05\/23\/activation-of-macrophage-trpm2-and-cd36-promotes-atherosclerosis\/","title":{"rendered":"Activation of macrophage TRPM2 and CD36 promotes atherosclerosis"},"content":{"rendered":"

Atherosclerosis is the major cause of ischemic heart disease and stroke, the leading causes of mortality worldwide.\u00a0To develop better therapies, Dr. Yue\u2019s group focuses on investigating the underlying mechanism of atherosclerosis, the root cause of cardiovascular diseases and brain stroke. The\u00a0prominent feature of\u00a0atherosclerosis is the formation of foam cells, the lipid-laden macrophages. Foam cells accelerate the progression of atherosclerosis by enhancing the inflammatory responses inside the arterial walls. Lipid uptake of macrophages is mainly mediated by CD36.\u00a0TRPM2 is a\u00a0heat-sensitive and calcium-permeable ion channel that is usually activated by oxidative stress conditions, and oxidative stress is also the prominent feature of\u00a0atherosclerosis.<\/p>\n

Recently, Pengyu Zong, a graduate student in Yue lab, discovered \u200bthat TRPM2 plays a critical role in the development and progression of\u00a0atherosclerosis by promoting CD36 activation in macrophages (as shown in the illustrating image).\u200b\u00a0Trpm2\u00a0<\/em>deletion inhibits macrophage infiltration, foam cell formation and subsequent pro-inflammatory activation. Both global and macrophage-specific\u00a0Trpm2\u00a0<\/em>deletion attenuates HFD-induced atherosclerosis.\u00a0Taken together, their studies\u00a0reveal\u00a0an important mechanism\u00a0for understanding atherogenesis, and suggest TRPM2 as a promising target for screening more effective therapies for\u00a0atherosclerosis.\u00a0\u00a0Moreover, CD36 is highly expressed in many other cell types, especially endothelial cells, suggesting that TRPM2-CD36 coupling may also contribute to the pathogenesis of endothelial-dysfunction-related diseases, such as Alzheimer disease and stroke.<\/p>\n

 <\/p>\n

Pengyu\u2019s work has recently been published in Nature Cardiovascular research(https:\/\/www.nature.com\/articles\/s44161-022-00027-7<\/a>; https:\/\/www.nature.com\/articles\/s44161-022-00037-5<\/a>). To read the press release published in UConn Today, please click here (https:\/\/today.uconn.edu\/2022\/03\/deleting-a-protein-in-mice-prevents-cardiovascular-disease\/<\/a>). Pengyu also won a travel award for attending Vascular Discovery meeting held from 05\/10-05\/14 at Seattle, WA (featured here).<\/p>\n

\"\"

 <\/p>\n","protected":false},"excerpt":{"rendered":"

Atherosclerosis is the major cause of ischemic heart disease and stroke, the leading causes of mortality worldwide.\u00a0To develop better therapies, Dr. Yue\u2019s group focuses on investigating the underlying mechanism of atherosclerosis, the root cause of cardiovascular diseases and brain stroke. The\u00a0prominent feature of\u00a0atherosclerosis is the formation of foam cells, the lipid-laden macrophages. Foam cells accelerate […]<\/p>\n","protected":false},"author":2772,"featured_media":5403,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"wds_primary_category":0,"footnotes":""},"categories":[3,5,1],"tags":[],"acf":[],"publishpress_future_action":{"enabled":false,"date":"2026-05-29 13:51:33","action":"change-status","newStatus":"draft","terms":[],"taxonomy":"category"},"_links":{"self":[{"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/posts\/5405"}],"collection":[{"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/users\/2772"}],"replies":[{"embeddable":true,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/comments?post=5405"}],"version-history":[{"count":7,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/posts\/5405\/revisions"}],"predecessor-version":[{"id":5417,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/posts\/5405\/revisions\/5417"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/media\/5403"}],"wp:attachment":[{"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/media?parent=5405"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/categories?post=5405"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/health.uconn.edu\/neuroscience\/wp-json\/wp\/v2\/tags?post=5405"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}