What this means
This review summarizes earlier studies on senescence, a state where cells stop dividing and release inflammatory signals. It suggests this state can help or harm the eye's surface, depending on the situation.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- A review of studies on eye surface disease, including cells in a dish, animals, and some people
- Kind of research
- A summary of earlier studies
The science
- Original title
- Cellular Senescence in Ocular Surface Diseases: Molecular Mechanisms and Therapeutic Perspectives.
- Authors
- Zhang L, Li S, Gao Q et al.
- Journal
- International journal of molecular sciences
- Published
- Oct 27, 2026
- Study type
- Review · in humans
- PMID
- 42941778 ↗
Abstract
Cellular senescence is characterized by stable cell-cycle arrest and a senescence-associated secretory phenotype (SASP). Recurrent desiccating, oxidative, ultraviolet, microbial, and immune-mediated insults may induce stress-induced premature senescence (SIPS) in ocular surface tissues. PubMed and Web of Science were searched from database inception to 30 June 2026. Primary human, animal, and in vitro studies were prioritized, and direct evidence of senescence was distinguished from indirect stress-related or SASP-like associations. The p53-p21CIP1-pRB and p16INK4a-pRB pathways mediate senescence-associated cell-cycle arrest. Reactive oxygen species (ROS)-p38 mitogen-activated protein kinase (p38 MAPK) and cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling act as stress-sensing and inflammatory pathways, whereas mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) contribute to SASP and metabolic regulation. Transient senescence may support wound repair and immune clearance, whereas persistent senescence may contribute to epithelial and endothelial dysfunction, tear-film instability, immune dysregulation, fibrosis, and extracellular matrix remodeling. Mechanistic support is strongest in selected experimental models; evidence in several human ocular surface disorders remains associative. Cellular senescence is a context-dependent contributor to ocular surface pathology. Senolytic and senomorphic strategies remain predominantly preclinical and require disease-, cell-, and stage-specific validation.
Zhang L, Li S, Gao Q et al. Cellular Senescence in Ocular Surface Diseases: Molecular Mechanisms and Therapeutic Perspectives. International journal of molecular sciences. 2026. doi:10.3390/ijms27209003. PMID: 42941778. https://pubmed.ncbi.nlm.nih.gov/42941778/
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