Evidence mapPaperPMID 40445334Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

lncRNA H19 as a molecular rheostat in autoimmunity: orchestrating miRNA-mediated gene regulation and immune cell reprogramming.

Thikra Majid Muhammed, Mahmood Yaseen Mukhlif, Ahmed Hossein, Renuka Jyothi S, Vishal Thakur, Swati Mishra, Ashish Singh Chauhan, Mahmood Hasen Shuhata, Mohammed Jawad Alnajar, Hayder Abdulhasan Hammoodi

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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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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.

Thikra Majid MuhammedBiology Department, College of Education for Pure Sciences, University of Anbar, Baghdad, Ramadi, 31001, Iraq.
Mahmood Yaseen MukhlifMedical Laboratory Techniques Department, College of Health and Medical Technology, University of Al Maarif, Anbar, Iraq. mahmoodyaseenmukhalif@gmail.com.
Ahmed HosseinDepartment of Medical Analysis, Medical Laboratory Technique College, the Islamic University, Najaf, Iraq.
Renuka Jyothi SDepartment of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Vishal ThakurCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
Swati MishraDepartment of Pharmacology, IMS and SUM Hospital, Siksha O Anusandhan (Deemed to be University), Bhubaneswar, Odisha, 751003, India.
Ashish Singh ChauhanUttaranchal Institute of Pharmaceutical Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, Uttarakhand, India.
Mahmood Hasen ShuhataAl-Hadi University College, Baghdad, 10011, Iraq.
Mohammed Jawad AlnajarDepartment of Pharmacy, Al-Nisour University College, Baghdad, Iraq.
Hayder Abdulhasan HammoodiMazaya University College, Nasiriyah, Dhi Qar, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The long non-coding RNA H19 (lncRNA H19) functions as a crucial regulator that controls various biological processes especially in immunological responses and autoimmune disease pathogenesis. Autoimmunity develops through complex interactions between genetic factors and environmental triggers and epigenetic changes which result in improper immune reactions against self-antigens. Research findings demonstrate that lncRNA H19 functions as a key regulator which controls immune cell behavior and controls inflammatory pathways and epigenetic regulatory mechanisms. The immune system dysregulation caused by H19 leads to changes in autoimmune disease progression and clinical symptom development. The balance between pro-inflammatory and anti-inflammatory cytokine production is controlled by lncRNA H19 through its interactions with NF-κB signaling cascade and multiple microRNA networks. The immunological tolerance mechanism depends on lncRNA H19 to control T cell differentiation through its regulation of regulatory T cells and T-helper 17-cell populations. The altered expression of lncRNA H19 in autoimmune diseases makes it an attractive subject for research as both a diagnostic biomarker and therapeutic target. This review summarizes recent findings to explain how lncRNA H19 functions in autoimmune disease immunopathogenesis and its therapeutic potential.

Indexed as

Autoimmune DiseasesAutoimmunityMicroRNAsRNA, Long NoncodingAnimalsGene Expression RegulationHumansH19 long non-coding RNAMicroRNAsRNA, Long NoncodingAutoimmune diseaseImmune systemLncRNA H19MiRNAMRNASignalling pathways

Identifiers

What Socratic 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 Socratic graph.