Mitochondria, aging, and cellular senescence: implications for scleroderma

M Bueno, A Papazoglou, E Valenzi, M Rojas… - Current rheumatology …, 2020 - Springer
M Bueno, A Papazoglou, E Valenzi, M Rojas, R Lafyatis, AL Mora
Current rheumatology reports, 2020Springer
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 …
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.
Summary
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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