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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Cellular Senescence in Ocular Surface Diseases: Molecular Mechanisms and Therapeutic Perspectives

  • Linkang Zhang1
  • Shipeng Li2
  • Qiao Gao1
  • Hongkun Zhang3
  • Hong Zhang1
  • Shudan Wang1
  1. 1Eye Hospital, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China
  2. 2Department of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, China
  3. 3Second Affiliated Hospital of Heilongjiang TCM University, Harbin 150001, China
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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.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026cellular,
  title = {{Cellular Senescence in Ocular Surface Diseases: Molecular Mechanisms and Therapeutic Perspectives}},
  author = {Linkang Zhang and Shipeng Li and Qiao Gao and Hongkun Zhang and Hong Zhang and Shudan Wang},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209003},
  url = {https://www.mdpi.com/1422-0067/27/20/9003},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Cellular Senescence in Ocular Surface Diseases: Molecular Mechanisms and Therapeutic Perspectives
AU  - Linkang Zhang
AU  - Shipeng Li
AU  - Qiao Gao
AU  - Hongkun Zhang
AU  - Hong Zhang
AU  - Shudan Wang
PY  - 2026
DA  - 2026/10/01
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209003
UR  - https://www.mdpi.com/1422-0067/27/20/9003
AB  - 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.
SN  - 1422-0067
ER  -