ArticleBurns & trauma2026
A novel CAVIN1/GAS5 axis suppresses skin fibrosis through mitochondrial fission-mediated attenuation of the TGF-β/Smad pathway.
Article in Burns & trauma, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Keloids, which are characterized by excessive collagen deposition and fibroblast hyperactivation, present significant therapeutic challenges because of their high recurrence rates and incompletely understood pathogenesis. The transforming growth factor-β (TGF-β) pathway is a central driver, but its upstream regulators in the development of skin fibrosis remain elusive. In this study, we aimed to identify novel upstream modulators of skin fibrosis and to elucidate the underlying molecular mechanisms by which these modulators regulate TGF-β signaling in keloid pathogenesis. Methods: We integrated results of transcriptomic and proteomic analyses of patient-derived keloid and normal skin tissues. Functional validation was performed by using primary keloid fibroblasts (KFs) with gain- and loss-of-function approaches, RNA immunoprecipitation sequencing (RIP-seq), and actinomycin D chase assays. Two independent bleomycin-induced skin fibrosis mouse models were employed for in vivo validation. Results: Multiomics profiling revealed that caveolae-associated protein 1 (CAVIN1) was consistently downregulated in keloids. CAVIN1 overexpression in KFs suppressed fibrotic phenotypes, including migration, invasion, collagen contraction, and extracellular matrix protein expression. Mechanistically, CAVIN1 directly bound to and stabilized the mitochondrial long noncoding RNA GAS5. This CAVIN1/GAS5 axis inhibited Drp1/Fis1-mediated mitochondrial fission and subsequent reactive oxygen species (ROS) production, leading to the attenuation of the canonical TGF-β/Smad2/3 signaling pathway. Critically, GAS5 silencing abrogated the antifibrotic effects of CAVIN1. Furthermore, database screening revealed that the histone deacetylase inhibitor vorinostat was a CAVIN1-upregulating compound. Both AAV-mediated CAVIN1 overexpression and vorinostat treatment significantly ameliorated skin fibrosis in the mouse models. Conclusions: Our study reports a novel CAVIN1/GAS5 axis that concurrently targets mitochondrial fission and the TGF-β/Smad pathway to suppress skin fibrosis. These findings not only reveal a previously unrecognized mechanistic link in keloid pathogenesis but also identify CAVIN1 as a promising therapeutic target, with vorinostat as a potential repurposable drug for treating fibrotic skin disorders.
Indexed as
Identifiers
What 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.