Illustration of an aging eye with cellular structures representing cataract-related proteins.

Can We Slow Down Cataracts? The Surprising Role of Cellular Aging

Samir D’Costa in Health & Wellness December 2025 • 4 min read.

"New research explores how proteins linked to cellular senescence might hold the key to preventing age-related cataracts."

Cataracts, characterized by the clouding of the eye's lens, are a leading cause of vision impairment globally, particularly among older adults. Age-related cataracts (ARC) are the most common type, encompassing nuclear, cortical, and posterior subcapsular forms. While the exact causes of ARC are complex and multifaceted, involving factors like age, genetics, and environmental exposures, a growing body of research points to the role of cellular aging processes.

Recent studies have focused on the potential involvement of cellular senescence—a state where cells stop dividing but remain metabolically active—in the development of cataracts. Senescent cells can accumulate in various tissues with age, releasing factors that contribute to inflammation and tissue dysfunction. This has led researchers to investigate specific markers of cellular senescence, such as senescence-associated beta-galactosidase (SA-β-gal) and senescence marker protein-30 (SMP-30), and their relationship to lens health.

A new study published in Medical Science Monitor has investigated the associations between SMP-30 and SA-β-gal expression with lens epithelial cell apoptosis (programmed cell death) in Chinese patients with age-related cataracts. The findings shed light on how these senescence markers might influence lens health and cataract development.

What Role Do SMP-30 and SA-β-gal Play in Cataract Development?

Illustration of an aging eye with cellular structures representing cataract-related proteins.

The study enrolled 145 age-related cataract patients, including 69 with nuclear cataracts and 76 with cortical cataracts. Lens epithelial cell samples were collected during cataract surgery, and the levels of SMP-30 and SA-β-gal were analyzed using immunohistochemical staining and real-time PCR. Additionally, a TUNEL assay was performed to assess the degree of lens epithelial cell apoptosis.

The research team compared protein and mRNA expression levels between the two cataract groups and analyzed how these senescence markers correlated with cell apoptosis. Key findings included:

SMP-30 protein expression was higher in the surrounding parts of the anterior lens capsule compared to the central part.
SA-β-gal positive rate was remarkably higher in the central part of the anterior lens capsule than in the surrounding part.
Nuclear cataract patients had elevated SMP-30 protein and mRNA expression levels but a decreased positive rate of SA-β-gal compared to cortical cataract patients.
Cortical cataract patients exhibited a significantly higher lens epithelial cell apoptosis rate compared to nuclear cataract patients.

These results suggest that both SMP-30 and SA-β-gal expressions are associated with lens epithelial cell apoptosis in nuclear and cortical cataracts. This indicates their possible involvement in the pathophysiology of age-related cataracts.

What Does This Mean for Future Cataract Treatment?

The identification of SMP-30 and SA-β-gal as potential players in lens epithelial cell apoptosis opens new avenues for exploring future cataract treatments. Further research is needed to fully understand the mechanisms by which these senescence markers influence cataract development and whether they can be targeted to prevent or slow down the progression of the disease. Larger studies are warranted to validate these findings and explore their implications for cataract prevention and treatment.

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Everything You Need To Know

What are the primary types of age-related cataracts (ARC)?

The most common type of cataracts is age-related cataracts (ARC). These include nuclear, cortical, and posterior subcapsular forms. The development of these cataracts is complex, influenced by factors like age, genetics, and environmental exposures. The research explores the role of cellular aging processes in these different types of ARC.

How are SMP-30 and SA-β-gal related to cataract development?

The study in *Medical Science Monitor* investigated the relationship between SMP-30 and SA-β-gal expressions and lens epithelial cell apoptosis in age-related cataract patients. The findings suggest that both SMP-30 and SA-β-gal are associated with lens epithelial cell apoptosis in nuclear and cortical cataracts, implying their involvement in the pathophysiology of age-related cataracts. Higher SMP-30 protein expression was observed in the surrounding parts of the anterior lens capsule, while SA-β-gal was more prevalent in the central part. Nuclear cataract patients showed elevated SMP-30 but decreased SA-β-gal, while cortical cataract patients had a higher rate of lens epithelial cell apoptosis.

What is cellular senescence and how does it relate to cataracts?

Cellular senescence is a state where cells stop dividing but remain metabolically active. Senescent cells accumulate with age and release factors that contribute to inflammation and tissue dysfunction. Research suggests a link between cellular senescence and the development of cataracts. The markers like senescence-associated beta-galactosidase (SA-β-gal) and senescence marker protein-30 (SMP-30) are investigated for their relationship to lens health and cataract development.

What were the key findings regarding SMP-30 and SA-β-gal in the study?

The study revealed several key findings. SMP-30 protein expression was higher in the surrounding parts of the anterior lens capsule compared to the central part. SA-β-gal positive rate was remarkably higher in the central part of the anterior lens capsule than in the surrounding part. Nuclear cataract patients had elevated SMP-30 protein and mRNA expression levels but a decreased positive rate of SA-β-gal compared to cortical cataract patients. Cortical cataract patients exhibited a significantly higher lens epithelial cell apoptosis rate compared to nuclear cataract patients. These results highlight the association between these markers and lens health.

How could the research on SMP-30 and SA-β-gal influence future cataract treatments?

The identification of SMP-30 and SA-β-gal as potential players in lens epithelial cell apoptosis opens new avenues for exploring future cataract treatments. Further research is needed to fully understand the mechanisms by which these senescence markers influence cataract development and whether they can be targeted to prevent or slow down the progression of the disease. This could potentially lead to new therapeutic strategies that target these senescence markers to prevent or treat cataracts. However, larger studies are needed to validate these findings and explore their implications for cataract prevention and treatment.