Evidence map›Paper›PMID 37443708›Full record

ReviewCells2023

p38γ MAPK Inflammatory and Metabolic Signaling in Physiology and Disease.

Xiao-Mei Qi, Guan Chen

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. p38γ and p38δ MAP kinases in inflammation.Biochemical Society transactions · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. SDS3 regulates microglial inflammation by modulating the expression of the upstream kinase ASK1 in the p38 MAPK signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
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

2 authors at 2 institutions in 1 country.

Xiao-Mei QiDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Guan ChenDepartment of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Medical College of Wisconsin · USMilwaukee VA Medical Center · US

Funding

NIH HHS CA245977VA I01 BX005066
6 · The paper itself

Abstract

p38γ MAPK (also called ERK6 or SAPK3) is a family member of stress-activated MAPKs and has common and specific roles as compared to other p38 proteins in signal transduction. Recent studies showed that, in addition to inflammation, p38γ metabolic signaling is involved in physiological exercise and in pathogenesis of cancer, diabetes, and Alzheimer's disease, indicating its potential as a therapeutic target. p38γphosphorylates at least 19 substrates through which p38γ activity is further modified to regulate life-important cellular processes such as proliferation, differentiation, cell death, and transformation, thereby impacting biological outcomes of p38γ-driven pathogenesis. P38γ signaling is characterized by its unique reciprocal regulation with its specific phosphatase PTPH1 and by its direct binding to promoter DNAs, leading to transcriptional activation of targets including cancer-like stem cell drivers. This paper will review recent findings about p38γ inflammation and metabolic signaling in physiology and diseases. Moreover, we will discuss the progress in the development of p38γ-specific pharmacological inhibitors for therapeutic intervention in disease prevention and treatment by targeting the p38γ signaling network.

Indexed as

Mitogen-Activated Protein Kinase 12Signal TransductionPhosphorylationMitogen-Activated Protein Kinase 12cancerp38γsignal transduction

Identifiers

PMID37443708
PMCPMC10341180
OpenAlexW4381663214

What Socratic 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 Socratic graph.