Marta Bueno1,2, Anna Papazoglou3, Eleanor Valenzi2, Mauricio Rojas2,4, Robert Lafyatis3, Ana L Mora5,6. 1. Department of Medicine, Aging Institute, University of Pittsburgh, 560 Bridgeside Point 1 Bldg.100 Technology Drive, Pittsburgh, PA, 15219, USA. 2. Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA. 3. Division of Rheumatology and Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, USA. 4. Dorothy and Richard Simmons Center for Interstitial Lung Diseases, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA. 5. Department of Medicine, Aging Institute, University of Pittsburgh, 560 Bridgeside Point 1 Bldg.100 Technology Drive, Pittsburgh, PA, 15219, USA. anamora@pitt.edu. 6. Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA. anamora@pitt.edu.
Abstract
PURPOSE OF REVIEW: The etiology of systemic sclerosis (SSc), which is a rare immune-mediated inflammatory disease characterized by vascular damage and fibrosis, is still unknown. However, different intrinsic (genetics) and extrinsic (environmental) factors play a part in the progression of the disease. This review focuses on the role of aging, mitochondrial dysfunction, and senescence in SSc. RECENT FINDINGS: Mitochondrial dysfunction and senescence have been linked to the age-related susceptibility to other interstitial lung diseases (ILD) such as idiopathic pulmonary fibrosis (IPF). SSc is not regarded as an age-related disease but does show a higher incidence of cardiac events, fibrosis, and mortality at older age. We provide an overview of the current status of the role of aging, mitochondrial dysfunction, and senescence in SSc. Further work is needed to validate some of these pathways in SSc and may allow for new therapeutic interventions focused on restoring mitochondrial homeostasis and the targeted removal of chronic-senescent cells.
PURPOSE OF REVIEW: The etiology of systemic sclerosis (SSc), which is a rare immune-mediated inflammatory disease characterized by vascular damage and fibrosis, is still unknown. However, different intrinsic (genetics) and extrinsic (environmental) factors play a part in the progression of the disease. This review focuses on the role of aging, mitochondrial dysfunction, and senescence in SSc. RECENT FINDINGS:Mitochondrial dysfunction and senescence have been linked to the age-related susceptibility to other interstitial lung diseases (ILD) such as idiopathic pulmonary fibrosis (IPF). SSc is not regarded as an age-related disease but does show a higher incidence of cardiac events, fibrosis, and mortality at older age. We provide an overview of the current status of the role of aging, mitochondrial dysfunction, and senescence in SSc. Further work is needed to validate some of these pathways in SSc and may allow for new therapeutic interventions focused on restoring mitochondrial homeostasis and the targeted removal of chronic-senescent cells.
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