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The Link Between Dysregulated Immunometabolism and Vascular Damage: Implications for the Development of Atherosclerosis in Systemic Lupus Erythematosus and Other Rheumatic Diseases.
Yennemadi, Anjali S; Jordan, Natasha; Diong, Sophie; Keane, Joseph; Leisching, Gina.
Afiliação
  • Yennemadi AS; A.S. Yennemadi, MSc, J. Keane, MD, G. Leisching, PhD, TB Immunology Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, School of Medicine, Trinity College Dublin, University of Dublin.
  • Jordan N; N. Jordan, PhD, Department of Rheumatology, St. James's Hospital.
  • Diong S; S. Diong, MD, Department of Dermatology, St. James's Hospital, Dublin, Ireland.
  • Keane J; A.S. Yennemadi, MSc, J. Keane, MD, G. Leisching, PhD, TB Immunology Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, School of Medicine, Trinity College Dublin, University of Dublin.
  • Leisching G; A.S. Yennemadi, MSc, J. Keane, MD, G. Leisching, PhD, TB Immunology Group, Department of Clinical Medicine, Trinity Translational Medicine Institute, School of Medicine, Trinity College Dublin, University of Dublin; gina.leisching@tcd.ie.
J Rheumatol ; 51(3): 234-241, 2024 Mar 01.
Article em En | MEDLINE | ID: mdl-38224981
ABSTRACT
A bimodal pattern of mortality in systemic lupus erythematosus (SLE) exists. Early-stage deaths are predominantly caused by infection, whereas later-stage deaths are mainly caused by atherosclerotic disease. Further, although SLE-related mortality has reduced considerably in recent years, cardiovascular (CV) events remain one of the leading causes of death in people with SLE. Accelerated atherosclerosis in SLE is attributed to both an increase in traditional CV risk factors and the inflammatory effects of SLE itself. Many of these changes occur within the microenvironment of the vascular-immune interface, the site of atherosclerotic plaque development. Here, an intimate interaction between endothelial cells, vascular smooth muscle cells, and immune cells dictates physiological vs pathological responses to a chronic type 1 interferon environment. Low-density neutrophils (LDNs) have also been implicated in eliciting vasculature-damaging effects at such lesion sites. These changes are thought to be governed by dysfunctional metabolism of immune cells in this niche due at least in part to the chronic induction of type 1 interferons. Understanding these novel pathophysiological mechanisms and metabolic pathways may unveil potential innovative pharmacological targets and therapeutic opportunities for atherosclerosis, as well as shed light on the development of premature atherosclerosis in patients with SLE who develop CV events.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doenças Reumáticas / Aterosclerose / Lúpus Eritematoso Sistêmico Tipo de estudo: Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Doenças Reumáticas / Aterosclerose / Lúpus Eritematoso Sistêmico Tipo de estudo: Risk_factors_studies Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article