Evidence map›Paper›PMID 39169436›Full record

ReviewAdvances in rheumatology (London, England)2024

Targeting Bruton's tyrosine kinase (BTK) as a signaling pathway in immune-mediated diseases: from molecular mechanisms to leading treatments.

Gita Manzari Tavakoli, Niloufar Yazdanpanah, Nima Rezaei

Abstract readReview
In one paragraph

Review in Advances in rheumatology (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Cardiovascular Toxicity of BTKi in Chronic B-Cell Malignancies.Reviews in cardiovascular medicine · 2026
    Review
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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

3 authors.

Gita Manzari TavakoliStudent's Scientific Research Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Niloufar YazdanpanahStudent's Scientific Research Center, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Nima RezaeiResearch Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. rezaei_nima@tums.ac.ir.ORCID 0000-0002-3836-1827

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bruton's tyrosine kinase (BTK), a nonreceptor tyrosine kinase, plays a remarkable role in the transmission and amplification of extracellular signals to intracellular signaling pathways. Various types of cells use the BTK pathway to communicate, including hematopoietic cells particularly B cells and T cells. The BTK pathway plays a role in controlling the proliferation, survival, and functions of B cells as well as other myeloid cells. First, second, and third-generation BTK inhibitors are currently being evaluated for the treatment of immune-mediated diseases in addition to B cell malignancies. In this article, the available evidence on the action mechanisms of BTK inhibitors is reviewed. Then, the most recent data obtained from preclinical studies and ongoing clinical trials for the treatment of autoimmune diseases, such as pemphigus vulgaris, pemphigus foliaceus, bullous pemphigoid, systemic lupus erythematosus, Sjögren's disease, rheumatoid arthritis, systemic sclerosis, multiple sclerosis, myasthenia gravis, and inflammatory diseases such as psoriasis, chronic spontaneous urticaria, atopic dermatitis, and asthma are discussed. In addition, adverse effects and complications associated with BTK inhibitors as well as factors predisposing patients to BTK inhibitors complications are discussed.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAutoimmune DiseasesPemphigusProtein Kinase InhibitorsSignal TransductionAdenineArthritis, RheumatoidAsthmaBenzamidesB-LymphocytesHumansImidazolesLupus Erythematosus, SystemicMultiple SclerosisMyasthenia GravisNitrilesacalabrutinibAdenineAgammaglobulinaemia Tyrosine KinaseBenzamidesBTK protein, humanevobrutinibibrutinibImidazolesNitrilesPiperidinesProtein Kinase InhibitorsProtein-Tyrosine KinasesPyrazinesPyrazolesPyrimidinesruxolitinibtirabrutinibzanubrutinibAutoimmune diseasesBruton's tyrosine kinaseBruton's tyrosine kinase inhibitorBTKBTKiImmune-mediated diseasesInflammatory diseases

Identifiers

PMID39169436
PMCPMC13488671

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.