Yudong Liu1, Mariana J Kaplan. 1. Systemic Autoimmunity Branch, Intramural Research Program, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
Abstract
PURPOSE OF REVIEW: The mechanisms leading to the development of premature atherosclerosis and vascular injury in systemic lupus erythematosus (SLE) remain to be fully elucidated. This is a comprehensive review of recent research developments related to the understanding of cardiovascular disease (CVD) in lupus. RECENT FINDINGS: SLE patients with lupus nephritis display significantly increased risk of myocardial infarction and CVD mortality than SLE patients without lupus nephritis. SLE disease-related parameters could be taken into consideration when calculating CVD risks. The type I interferon pathway is detrimental to the vasculature and may contribute to the development of insulin resistance. The level of low-density granulocytes, a distinct subset of proinflammatory neutrophils present in SLE, was independently associated with coronary plaque burden and endothelial dysfunction. Invariant natural killer T cells may promote an atheroprotective effect in SLE patients with asymptomatic atherosclerotic plaques. Oxidized lupus high-density lipoprotein promotes proinflammatory responses in macrophages. SUMMARY: Recent discoveries have further strengthened the critical role of SLE-related immune dysregulation and metabolic disturbances in promoting accelerated CVD. Understanding how these pathogenic factors promote vascular injury may provide better molecular candidates for therapeutic targeting, and ultimately to improve CVD outcomes.
PURPOSE OF REVIEW: The mechanisms leading to the development of premature atherosclerosis and vascular injury in systemic lupus erythematosus (SLE) remain to be fully elucidated. This is a comprehensive review of recent research developments related to the understanding of cardiovascular disease (CVD) in lupus. RECENT FINDINGS:SLEpatients with lupus nephritis display significantly increased risk of myocardial infarction and CVD mortality than SLEpatients without lupus nephritis. SLE disease-related parameters could be taken into consideration when calculating CVD risks. The type I interferon pathway is detrimental to the vasculature and may contribute to the development of insulin resistance. The level of low-density granulocytes, a distinct subset of proinflammatory neutrophils present in SLE, was independently associated with coronary plaque burden and endothelial dysfunction. Invariant natural killer T cells may promote an atheroprotective effect in SLEpatients with asymptomatic atherosclerotic plaques. Oxidized lupus high-density lipoprotein promotes proinflammatory responses in macrophages. SUMMARY: Recent discoveries have further strengthened the critical role of SLE-related immune dysregulation and metabolic disturbances in promoting accelerated CVD. Understanding how these pathogenic factors promote vascular injury may provide better molecular candidates for therapeutic targeting, and ultimately to improve CVD outcomes.
Authors: Dalton Bertolim Précoma; Gláucia Maria Moraes de Oliveira; Antonio Felipe Simão; Oscar Pereira Dutra; Otávio Rizzi Coelho; Maria Cristina de Oliveira Izar; Rui Manuel Dos Santos Póvoa; Isabela de Carlos Back Giuliano; Aristóteles Comte de Alencar Filho; Carlos Alberto Machado; Carlos Scherr; Francisco Antonio Helfenstein Fonseca; Raul Dias Dos Santos Filho; Tales de Carvalho; Álvaro Avezum; Roberto Esporcatte; Bruno Ramos Nascimento; David de Pádua Brasil; Gabriel Porto Soares; Paolo Blanco Villela; Roberto Muniz Ferreira; Wolney de Andrade Martins; Andrei C Sposito; Bruno Halpern; José Francisco Kerr Saraiva; Luiz Sergio Fernandes Carvalho; Marcos Antônio Tambascia; Otávio Rizzi Coelho-Filho; Adriana Bertolami; Harry Correa Filho; Hermes Toros Xavier; José Rocha Faria-Neto; Marcelo Chiara Bertolami; Viviane Zorzanelli Rocha Giraldez; Andrea Araújo Brandão; Audes Diógenes de Magalhães Feitosa; Celso Amodeo; Dilma do Socorro Moraes de Souza; Eduardo Costa Duarte Barbosa; Marcus Vinícius Bolívar Malachias; Weimar Kunz Sebba Barroso de Souza; Fernando Augusto Alves da Costa; Ivan Romero Rivera; Lucia Campos Pellanda; Maria Alayde Mendonça da Silva; Aloyzio Cechella Achutti; André Ribeiro Langowiski; Carla Janice Baister Lantieri; Jaqueline Ribeiro Scholz; Silvia Maria Cury Ismael; José Carlos Aidar Ayoub; Luiz César Nazário Scala; Mario Fritsch Neves; Paulo Cesar Brandão Veiga Jardim; Sandra Cristina Pereira Costa Fuchs; Thiago de Souza Veiga Jardim; Emilio Hideyuki Moriguchi; Jamil Cherem Schneider; Marcelo Heitor Vieira Assad; Sergio Emanuel Kaiser; Ana Maria Lottenberg; Carlos Daniel Magnoni; Marcio Hiroshi Miname; Roberta Soares Lara; Artur Haddad Herdy; Cláudio Gil Soares de Araújo; Mauricio Milani; Miguel Morita Fernandes da Silva; Ricardo Stein; Fernando Antonio Lucchese; Fernando Nobre; Hermilo Borba Griz; Lucélia Batista Neves Cunha Magalhães; Mario Henrique Elesbão de Borba; Mauro Ricardo Nunes Pontes; Ricardo Mourilhe-Rocha Journal: Arq Bras Cardiol Date: 2019-11-04 Impact factor: 2.000