Current rheumatology reports · 2020
Mitochondria, Aging, and Cellular Senescence: Implications for Scleroderma.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Bueno Marta, Papazoglou Anna, Valenzi Eleanor, Rojas Mauricio, Lafyatis Robert, Mora Ana L
Аннотация
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.
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.