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We propose that colchicine's antiplatelet effects primarily target collagen-induced platelet activation <jats:italic>via<\/jats:italic> the collagen receptor, glycoprotein (GP)VI, which is critical for arterial thrombosis formation. In settings such as stroke and MI, GPVI signaling is upregulated. We have demonstrated <jats:italic>in vitro<\/jats:italic> that therapeutic concentrations of colchicine lead to a decrease in collagen-induced platelet aggregation and alter GPVI signaling. Clinical studies of colchicine given for 6 months lead to a significant reduction in serum GPVI levels in CAD patients, which may ameliorate thrombotic risk. Future evaluation of the effects of colchicine in clinical trials should include assessment of its effects on collagen-mediated platelet activation, and consideration be given to quantifying the contribution of such antiplatelet effects additional to the known anti-inflammatory effects of colchicine.<\/jats:p>","DOI":"10.3389\/fcvm.2022.1104744","type":"journal-article","created":{"date-parts":[[2023,1,19]],"date-time":"2023-01-19T06:04:40Z","timestamp":1674108280000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":14,"title":["Perspective: Collagen induced platelet activation via the GPVI receptor as a primary target of colchicine in cardiovascular disease"],"prefix":"10.3389","volume":"9","author":[{"given":"Gabrielle J.","family":"Pennings","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline 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