Senescent synovial fibroblasts accumulate prematurely in rheumatoid arthritis tissues and display an enhanced inflammatory phenotype

Cells exhibiting strong p16INK4a promoter activation in vivo display features of senescence

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Length‐independent telomere damage drives post‐mitotic cardiomyocyte senescence

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Multilineage-differentiating stress-enduring (Muse)-like cells exist in synovial tissue

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Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment

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Cellular senescence mediates fibrotic pulmonary disease

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Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice

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Paclitaxel inhibits cell proliferation and collagen lattice contraction via TGF-β signaling pathway in human tenon's fibroblasts in vitro

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Transplanted Senescent Cells Induce an Osteoarthritis-Like Condition in Mice

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Naturally occurring p16Ink4a-positive cells shorten healthy lifespan

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Inflammaging decreases adaptive and innate immune responses in mice and humans

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The number of p16INK4a positive cells in human skin reflects biological age

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Lamin B1 loss is a senescence-associated biomarker

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Protocols to detect senescence-associated beta-galactosidase (SA-βgal) activity, a biomarker of senescent cells in culture and in vivo

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Senescence-Associated Secretory Phenotypes Reveal Cell-Nonautonomous Functions of Oncogenic RAS and the p53 Tumor Suppressor

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