ArticleInvestigative ophthalmology & visual science2025
PGC1A Restores Mitochondrial Health to Attenuate EMT During Lens Epithelial Fibrosis via Regulating TFAM.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- A Systems View of Posterior Capsule Opacification: TGF-β/ROS Signaling, Mitochondrial Homeostasis, and Injury/Aging Cues-Therapeutic Opportunities.Investigative ophthalmology & visual science · 2026Review
- Gigantol Preserves Lens Biophysical Homeostasis by Restoring Cytoskeletal Integrity and Membrane Fluidity in a Diabetic Cataract Model.International journal of molecular sciences · 2026Article
- Environmental enrichment as a mitochondria-targeting systems strategy across neurodegenerative diseases and retinal dystrophies.Frontiers in neuroscience · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) is a predominant pathological driver for fibrotic cataracts. This study explores the role and mechanism of peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1A), a key mitochondrial regulator, in EMT of LECs. Methods: RNA-sequencing analysis was applied to reveal biological changes during human lens epithelial fibrosis. Primary rabbit LECs were treated with TGFβ2 to induce EMT. Mitochondrial alterations were evaluated by MitoTracker staining, transmission electron microscopy, mitochondrial membrane potential assay, ATP content assay, and reactive oxygen species (ROS) assay. Loss- and gain-of-function studies were performed to uncover roles and mechanisms of PGC1A in EMT of LECs. Changes of PGC1A, EMT markers, and mitochondrial regulators were analyzed by Western blot, immunofluorescence staining, and RT-qPCR. Cell migration was assessed using the cell scratch assay. Ex vivo whole rat lenses were treated with TGFβ2 to induce fibrotic cataract to evaluate the potential therapeutic effect of PGC1A on lens fibrosis. Lens epithelial fibrosis was examined by hematoxylin and eosin (H&E) and immunofluorescence staining. Results: PGC1A was decreased with significant mitochondrial dysfunction during TGFβ2-induced EMT of LECs. PGC1A silencing promoted EMT by enhancing TGFβ2-Smad2/3 signaling, accelerating subcapsular fibrotic plaque formation. PGC1A upregulation protected LECs from TGFβ2-induced EMT by restoring mitochondrial health and energy metabolism. Mechanistically, PGC1A inhibition decreased mitochondrial transcription factor (TFAM), which mediated protective effects of PGC1A on mitochondria and LECs. Further, ZLN005, a PGC1A agonist, attenuated fibrotic lens opacity via preventing LECs from EMT. Conclusions: PGC1A safeguards LECs against EMT by restoring TFAM-mediated mitochondrial energy metabolism under TGFβ2 stress, offering potential targets for the treatment of lens epithelial fibrosis.
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