ReviewEuropean journal of medical research2025
The role of HDAC6 in fibrosis: a novel and effective therapy strategy.
Review in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Reconstructing AF-associated atrial fibrosis: Patient-specific iPSC models, fit-for-purpose atrial microphysiological systems, and nanomedicine.Materials today. Bio · 2026Review
- Fibrotic Disease of the Skin and Lung: Shared Pathways, Environmental Drivers, and Therapeutic Opportunities in a Changing Climate.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Fibrosis is the usual pathological process observed across a broad spectrum of diseases. The mechanisms of fibrosis involve various cells and signaling pathways. Epigenetic regulation, such as histone acetylation, is one of the mechanisms. Among histone deacetylases (HDACs), histone deacetylase 6 (HDAC6) is particularly unique due to its two-domain structure and its presence in the cytoplasm. Apart from its well-known role as a histone modifier, HDAC6 interacts with multiple non-histone substrates, including α-tubulin, heat-shock protein 90 (HSP90), peroxiredoxins, and TGF-β. It also interacts with ubiquitin through noncatalytic functions. Elevated expression of HDAC6 has been observed in fibrotic diseases. Fibrosis is closely related to inflammation. Given that HDAC6 plays the unique link role in both fibrosis process and inflammation, HDAC6 inhibitors represent a new and effective maneuver for addressing fibrotic diseases. In this paper, we review recent advances in understanding the role of HDAC6 in fibrotic diseases affecting multiple organs, including the lung, heart, liver, kidney, and peritoneum. We also examine the effects of HDAC6 inhibitors, providing a valuable reference for future research into fibrosis mechanisms and therapeutic drug development.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.