The Nature Aging paper examines chaperone-mediated autophagy (CMA), a pathway that sends selected proteins to lysosomes for degradation. In mice, blocking CMA in macrophages increased senescent-cell accumulation and delayed wound healing. A small-molecule CMA activator reduced senescent-cell burden across multiple tissues and eased disease severity in a pulmonary-fibrosis model. The findings are preclinical and do not establish safety or effectiveness in humans.
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