ReviewApoptosis : an international journal on programmed cell death2025
Exploiting autophagy and related pathways: pioneering new horizons in cataract therapy.
Review in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Expression and mechanistic roles of long non-coding RNAs in diabetic cataract: a systematic review and meta-analysis.Biology direct · 2026Pooled it
- MAM-Localized MANF Counteracts Microinflammatory Stress to Attenuate Mitochondrial Dysfunction and Cataractogenesis in High Myopia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cataract: Surgery first - is there still room for basic research?Advances in ophthalmology practice and researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a critical catabolic pathway that facilitates the degradation of intracellular components through lysosomal activity, originally recognized for its role in nutrient recycling during starvation. Recent research has expanded our understanding of autophagy, revealing its involvement in various physiological processes essential for cellular, tissue, and organismal homeostasis. Dysregulation of autophagy has been linked to numerous diseases, including ocular conditions such as cataracts. In human lens fibers, autophagic vesicles containing mitochondria or mitochondrial fragments have been identified, underscoring the importance of autophagy in maintaining lens integrity and transparency. Disruptions in organelle elimination can lead to increased reactive oxygen species (ROS), altering lens homeostasis and contributing to cataract formation. Recent studies have highlighted the complex interplay between autophagy and lens epithelial cells (LECs) in both age-related and diabetic cataract development. In age-related cataracts, increased autophagic activity coincides with elevated apoptosis in LECs, suggesting a bidirectional regulatory role of autophagy in cellular senescence. Additionally, the degradation of SQSTM1/p62 during oxidative stress implicates autophagy in the apoptotic processes associated with senile cataracts. In diabetic cataracts, high glucose levels disrupt the relationship between autophagy and epithelial-mesenchymal transition (EMT) in LECs via the Notch signaling pathway, leading to impaired autophagic function and subsequent cataractogenesis. These findings indicate that autophagy dysregulation is a significant contributor to the pathophysiology of various cataract types. Future research should focus on exploring the therapeutic potential of modulating autophagy to prevent or treat cataracts, investigating specific signaling pathways involved, and identifying biomarkers for early detection. By elucidating the molecular mechanisms underlying autophagy's role in cataract formation, novel targeted therapies may emerge, providing hope for improved management and prevention of this prevalent ocular pathology.
Indexed as
Identifiers
40634815What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.