ReviewBiochemistry and biophysics reports2026
Crucial involvement of transforming growth factor beta (TGF-β)/Smad signaling regulation by miR-204-5p in cataract and posterior capsular opacification.
Review in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Worldwide, cataracts remain the leading cause of irreversible blindness, primarily driven by age-related changes and free radical-mediated lens damage. Posterior capsular opacification (PCO) is a common complication following cataract surgery, arising from aberrant proliferation and epithelial-mesenchymal transition (EMT) of residual lens epithelial cells (LECs). The transforming growth factor-β (TGF-β)/Smad signaling cascade is among the most critical pathways underlying both cataractogenesis and PCO, as it drives EMT and subsequent fibrotic alterations. MicroRNAs have emerged as key regulators of ocular homeostasis, with miR-204-5p being particularly relevant. Highly expressed in the lens, miR-204-5p has been shown to target TGFBR2, a core component of the TGF-β/Smad pathway, and thereby suppress downstream signaling. Downregulation of miR-204-5p appears to enhance TGF-β signaling, which may contribute to lens fibrosis and opacification during cataract development or after surgery. This article reviews current understanding of the interplay between miR-204-5p and the TGF-β/Smad signaling pathway in LECs, focusing on their roles in EMT and fibrotic progression. We also highlight experimental evidence supporting miR-204-5p as a promising candidate for PCO prevention. Emerging evidence also suggests that miR-204-5p regulates oxidative stress and mitochondrial homeostasis through additional targets in lens epithelial cells, highlighting its broader therapeutic potential. Elucidating crosstalk between signaling and epigenetic regulation in LEC biology opens new avenues for non-surgical management of cataracts and PCO. This review underscores the need for further research into miRNA-mediated modulation of fibrotic signaling, establishing this as an innovative and promising direction in molecular ophthalmic therapy. Clinical trial number: not applicable.
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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.