Konstantinos Ntelis1, Dimitrios Bogdanos2, Theodoros Dimitroulas3, Lazaros Sakkas2, Dimitrios Daoussis4. 1. Department of Rheumatology, Agios Andreas Hospital, Patras, Greece. 2. Department of Rheumatology, Faculty of Medicine, School of Health Sciences, University of Thessaly, 41 110, Larissa, Greece. 3. 4th Department of Internal Medicine Hippokration Hospital, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece. 4. Department of Internal Medicine, Division of Rheumatology, Patras University Hospital, 26504 Rion, Patras, Greece. jimdaoussis@hotmail.com.
Abstract
PURPOSE OF REVIEW: Platelets are no longer recognized solely as cell fragments regulating hemostasis. They have pleiotropic functions and they are linked directly or indirectly with the three cornerstones of systemic sclerosis (SSc): vasculopathy, autoimmunity, and fibrosis. In this review, we summarize the current knowledge on the potential role of platelets in the pathogenesis of SSc. RECENT FINDINGS: Experimental evidence suggests that vasculopathy, a universal and early finding in SSc, may activate platelets which subsequently release several profibrotic mediators such as serotonin and transforming growth factor β (TGFβ). Platelets may also cross-react with the endothelium leading to the release of molecules, such as thymic stromal lymphopoietin (TSLP), that may trigger fibrosis or sustain vascular damage. Finally, activated platelets express CD40L and provide costimulatory help to B cells, something that may facilitate the breach in immune tolerance. Preclinical studies point to the direction that platelets are actively involved in SSc pathogenesis. Targeting platelets may be an attractive therapeutic approach in SSc.
PURPOSE OF REVIEW: Platelets are no longer recognized solely as cell fragments regulating hemostasis. They have pleiotropic functions and they are linked directly or indirectly with the three cornerstones of systemic sclerosis (SSc): vasculopathy, autoimmunity, and fibrosis. In this review, we summarize the current knowledge on the potential role of platelets in the pathogenesis of SSc. RECENT FINDINGS: Experimental evidence suggests that vasculopathy, a universal and early finding in SSc, may activate platelets which subsequently release several profibrotic mediators such as serotonin and transforming growth factor β (TGFβ). Platelets may also cross-react with the endothelium leading to the release of molecules, such as thymic stromal lymphopoietin (TSLP), that may trigger fibrosis or sustain vascular damage. Finally, activated platelets express CD40L and provide costimulatory help to B cells, something that may facilitate the breach in immune tolerance. Preclinical studies point to the direction that platelets are actively involved in SSc pathogenesis. Targeting platelets may be an attractive therapeutic approach in SSc.
Authors: José Alvaro Lomelí-Nieto; José Francisco Muñoz-Valle; Christian Johana Baños-Hernández; José Eduardo Navarro-Zarza; Juliana Marisol Godínez-Rubí; Samuel García-Arellano; María Guadalupe Ramírez-Dueñas; Isela Parra-Rojas; Arisbeth Villanueva-Pérez; Jorge Hernández-Bello Journal: Clin Exp Med Date: 2022-05-29 Impact factor: 3.984
Authors: Mina K Chung; David A Zidar; Michael R Bristow; Scott J Cameron; Timothy Chan; Clifford V Harding; Deborah H Kwon; Tamanna Singh; John C Tilton; Emily J Tsai; Nathan R Tucker; John Barnard; Joseph Loscalzo Journal: Circ Res Date: 2021-04-15 Impact factor: 17.367