Evidence map›Paper›PMID 37476157›Full record

ReviewFrontiers in cell and developmental biology2023

Fibrosis-the tale of H3K27 histone methyltransferases and demethylases.

Morgan D Basta, Svetlana Petruk, Alexander Mazo, Janice L Walker

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Epidrugs in cancer: mechanisms, applications, and future direction.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  2. Review
  3. Review
  4. Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Morgan D BastaDepartment of Pathology and Genomic Medicine, Thomas Jefferson University, Philadelphia, PA, United States.
Svetlana PetrukDepartment of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, United States.
Alexander MazoDepartment of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, United States.
Janice L WalkerDepartment of Pathology and Genomic Medicine, Thomas Jefferson University, Philadelphia, PA, United States.
Thomas Jefferson University · US

Funding

TRANSCRIPTIONAL REGULATION BY EPIGENETIC FACTORSR01GM075141 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI MAZO, ALEXANDER M · 2005 to 2021
$4.9M
Training in Tissue Engineering and Regenerative MedicineT32AR052273 · NIAMS · THOMAS JEFFERSON UNIVERSITY · PI SHAPIRO, IRVING M · 2006 to 2020
$3.3M
Structure of post-replicative chromatin during cell reprogramming in fibrotic diseaseR01EY026159 · NEI · THOMAS JEFFERSON UNIVERSITY · PI MAZO, ALEXANDER M, WALKER, JANICE LYNN · 2017 to 2020
$1.6M
NEI NIH HHS R01 EY026159NIAMS NIH HHS T32 AR052273NIGMS NIH HHS R01 GM075141
6 · The paper itself

Abstract

Fibrosis, or excessive scarring, is characterized by the emergence of alpha-smooth muscle actin (αSMA)-expressing myofibroblasts and the excessive accumulation of fibrotic extracellular matrix (ECM). Currently, there is a lack of effective treatment options for fibrosis, highlighting an unmet need to identify new therapeutic targets. The acquisition of a fibrotic phenotype is associated with changes in chromatin structure, a key determinant of gene transcription activation and repression. The major repressive histone mark, H3K27me3, has been linked to dynamic changes in gene expression in fibrosis through alterations in chromatin structure. H3K27-specific homologous histone methylase (HMT) enzymes, Enhancer of zeste 1 and 2 (EZH1, EZH2), which are the alternative subunits of the Polycomb Repressive Complex 2 (PRC2) and demethylase (KDM) enzymes, Ubiquitously transcribed tetratricopeptide repeat, X chromosome (UTX), and Lysine demethylase 6B (KDM6B), are responsible for regulating methylation status of H3K27me3. In this review, we explore how these key enzymes regulate chromatin structure to alter gene expression in fibrosis, highlighting them as attractive targets for the treatment of fibrosis.

Indexed as

chromatinepigeneticsextracellular matrixEZH1EZH2fibrosismyofibroblastUTX

Identifiers

PMID37476157
PMCPMC10354294
OpenAlexW4383224595

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.