Evidence map›Paper›PMID 40198399›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

Targeting EZH2 in autoimmune diseases: unraveling epigenetic regulation and therapeutic potential.

Hashem Ahmed Abu Harirah, Mohammed Hashim Mohammed, Sami Ahmed Zaher Basha, Subasini Uthirapathy, Subbulakshmi Ganesan, Aman Shankhyan, Girish Chandra Sharma, Anita Devi, Abed J Kadhim, Naher H S

Abstract readReview
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In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Hashem Ahmed Abu HarirahMedical Laboratory Department, Faculty of Allied Medical Sciences, Zarqa University, Zarqa, Jordan. hharirah@zu.edu.jo.
Mohammed Hashim MohammedMedical Laboratory Techniques Department, College of Health and Medical Technology, Al-Maarif University, Anbar, Iraq. Muhammad.hashem@uoa.edu.iq.
Sami Ahmed Zaher BashaPhysical Therapy Department, Faculty of Allied Medical Sciences, Zarqa University, Zarqa, Jordan.
Subasini UthirapathyPharmacy Department, Tishk International University, Kurdistan Region, Erbil, Iraq.
Subbulakshmi GanesanDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to Be University), Bangalore, Karnataka, India.
Aman ShankhyanCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
Girish Chandra SharmaDepartment of Applied Sciences-Chemistry, NIMS Institute of Engineering & Technology, NIMS University Rajasthan, Jaipur, India.
Anita DeviDepartment of Chemistry, Chandigarh Engineering College, Chandigarh Group of Colleges Jhanjeri, Mohali, 140307, Punjab, India.
Abed J KadhimDepartment of Medical Engineering, Al-Nisour University College, Baghdad, Iraq.
Naher H SLaboratories Techniques Department, College of Health and Medical Techniques, Al-Mustaqbal University, 51001, Babylon, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Approximately 8-10% of the global population is affected by autoimmune diseases (ADs), which encompass a wide array of idiopathic conditions resulting from dysregulated immune responses. The enzymatic component of the polycomb-repressive complex 2 (PRC2), enhancer of zeste homolog 2 (EZH2, also referred to as KMT6), functions as a methyltransferase possessing a SET domain that plays crucial roles in epigenetic regulation, explicitly facilitating the methylation of histone H3 at lysine 27. Notably, EZH2 is catalytically inactive and requires association with EED and SUZ12 to form an active PRC2 complex. Hyperactivation of EZH2 has been implicated in various malignancies, prompting the development of EZH2 inhibitors as therapeutic agents for several cancers, including lymphoma, prostate, breast, and colon cancer. The application of EZH2-targeting therapies has also been explored in the context of autoimmune diseases. While there have been advancements in certain ADs, responses can vary significantly, as evidenced by mixed outcomes in cases such as inflammatory bowel disease. Consequently, the dual role of EZH2 and the therapeutic potential of its inhibitors in the treatment of ADs remain nascent fields of study. This review will elucidate the interplay between EZH2 and autoimmune diseases, highlighting emerging insights and therapeutic avenues.

Indexed as

Autoimmune DiseasesEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticAnimalsHumansMolecular Targeted TherapyEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanAutoimmunityEpigenetic regulationEZH2IBD; SLEInhibitorTreatment

Identifiers

PMID40198399

What OpenQuestion holds

Textmetadata
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.