Open AccessMechanisms and therapeutic implications of cellular senescence in osteoarthritis
Author(s) -
Philip Coryell,
Brian O. Diekman,
Richard F. Loeser
Publication year - 2020
Publication title -
nature reviews. rheumatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.683
H-Index - 137
eISSN - 1759-4804
pISSN - 1759-4790
DOI - 10.1038/s41584-020-00533-7
Subject(s) - senescence , osteoarthritis , phenotype , pathogenesis , oxidative stress , disease , medicine , mechanism (biology) , cartilage , biology , bioinformatics , immunology , microbiology and biotechnology , pathology , gene , genetics , anatomy , philosophy , alternative medicine , epistemology
The development of osteoarthritis (OA) correlates with a rise in the number of senescent cells in joint tissues, and the senescence-associated secretory phenotype (SASP) has been implicated in cartilage degradation and OA. Age-related mitochondrial dysfunction and associated oxidative stress might induce senescence in joint tissue cells. However, senescence is not the only driver of OA, and the mechanisms by which senescent cells contribute to disease progression are not fully understood. Furthermore, it remains uncertain which joint cells and SASP-factors contribute to the OA phenotype. Research in the field has looked at developing therapeutics (namely senolytics and senomorphics) that eliminate or alter senescent cells to stop disease progression and pathogenesis. A better understanding of how senescence contributes to joint dysfunction may enhance the effectiveness of these approaches and provide relief for patients with OA.