Evidence map›Paper›PMID 42105167›Full record

ReviewMolecular biology reports2026

The JAK/STAT pathway: key mechanism in gene activation, disease regulation, and emerging therapeutic targets.

Jehan Mohamed, Habiba Ezat, Rana Abdelrahman, Rowana Abdelaziz, Reem Ayman, El-Khawaga Oy, Raghda W Magar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2026. 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. Review
  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

7 authors.

Jehan MohamedFaculty of Science, Department of Applied Biochemistry and Molecular Biology, Mansoura University, Mansoura, Egypt.
Habiba EzatFaculty of Science, Department of Applied Biochemistry and Molecular Biology, Mansoura University, Mansoura, Egypt.
Rana AbdelrahmanFaculty of Science, Department of Applied Biochemistry and Molecular Biology, Mansoura University, Mansoura, Egypt.
Rowana AbdelazizFaculty of Science, Department of Applied Biochemistry and Molecular Biology, Mansoura University, Mansoura, Egypt.
Reem AymanFaculty of Science, Department of Applied Biochemistry and Molecular Biology, Mansoura University, Mansoura, Egypt.
El-Khawaga OyFaculty of Science, Department of Applied Biochemistry and Molecular Biology, Mansoura University, Mansoura, Egypt.
Raghda W MagarTransplantation Immunology Department, Urology and Nephrology Center, Mansoura University, Mansoura, Egypt. Raghda_magar_uns@mans.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway is a fundamental intracellular mechanism that mediates cytokine and growth factor signaling. Dysregulation of this pathway through genetic mutations, polymorphisms, or persistent activation has been strongly associated with autoimmune diseases, inflammatory disorders, and a wide range of hematologic and solid malignancies. Consequently, the JAK/STAT pathway has emerged as a major therapeutic and diagnostic target in precision medicine. This review synthesizes evidence from experimental, translational, and clinical studies addressing the molecular structure, activation mechanisms, and regulatory control of JAK and STAT proteins. Aberrant JAK/STAT signaling contributes significantly to the pathogenesis of autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus, as well as malignancies including myeloproliferative neoplasms, lymphomas, and breast cancer. Somatic mutations, transcriptional activation signatures, and phosphorylated STAT proteins serve as valuable diagnostic and prognostic biomarkers. JAK inhibitors, including ruxolitinib and tofacitinib, demonstrate clinical efficacy; however, treatment resistance, adverse effects, and incomplete disease modification remain significant challenges. The involvement of JAK/STAT signaling in metabolic, cardiovascular, and neuroinflammatory diseases remains insufficiently explored. Predictive biomarkers for patient stratification and long-term treatment outcomes are not yet fully established. LIMITATION: This review is limited by reliance on heterogeneous published data and the scarcity of long-term clinical trials validating biomarker utility and resistance mechanisms. This review uniquely integrates the molecular structure, regulatory mechanisms, diagnostic biomarkers, therapeutic targeting, and resistance mechanisms of the JAK/STAT pathway across autoimmune diseases and malignancies.

conclusionThe JAK/STAT pathway is a central regulator of immune and inflammatory signaling with broad clinical relevance. The continued integration of molecular diagnostics, novel STAT-targeted agents, and combination therapies is essential for improving therapeutic precision and clinical outcomes.

Indexed as

Janus KinasesSTAT Transcription FactorsAnimalsAutoimmune DiseasesHumansJanus Kinase InhibitorsNeoplasmsSignal TransductionJanus Kinase InhibitorsJanus KinasesSTAT Transcription FactorsJanus kinase (JAK)Signal transducers and activators of transcription (STAT)

Identifiers

PMID42105167

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.