Evidence map›Paper›PMID 41388865›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.

Lillian Schulz, Abby E Young, Fang Liu, Sanjana Gattineni, Sneha S Ghosh, Eugene Douglass, Heike Kroeger, S Priya Narayanan, Neil J Grimsey

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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. Atypical p38 Kinase Signaling in Retinal Vascular Damage and Recovery.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    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

9 authors.

Lillian SchulzDepartment of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.
Abby E YoungDepartment of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.
Fang LiuClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia, USA.
Sanjana GattineniDepartment of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.
Sneha S GhoshDepartment of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.
Eugene DouglassDepartment of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.
Heike KroegerDepartment of Cellular Biology, University of Georgia, Athens, Georgia, USA.
S Priya NarayananClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia, USA.
Neil J GrimseyDepartment of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.ORCID https://orcid.org/0000-0002-0481-4920

Funding

Mechanisms of neurodegeneration in diabetic retinopathy: Role of spermine oxidaseR01EY028569 · NEI · UNIVERSITY OF GEORGIA · PI NARAYANAN, PRIYA · 2018 to 2023
$1.8M
HHS|NIH|National Eye Institute (NEI) 1R21EY03469101A1NEI NIH HHS R01 EY028569
6 · The paper itself

Abstract

Despite the life-changing impact of anti-VEGF therapies, vascular retinopathies continue to affect millions of patients worldwide. To better understand disease progression, it is essential to define alternative mechanisms that contribute to retinal vascular dysregulation. Mitogen-activated protein kinase (MAPK) p38 plays a significant role in regulating vascular homeostasis, angiogenesis, and retinal disease progression, yet effective therapeutic targeting remains elusive. An alternative atypical p38 signaling pathway is mediated by interaction with the adaptor protein TGF-beta activated kinase 1, binding protein 1 (TAB1). Atypical p38 can be activated by ischemia or by inflammatory G protein-coupled receptors (GPCRs) to regulate inflammation and vascular homeostasis. However, atypical signaling has not been investigated in the context of vascular retinopathies, specifically oxygen-induced retinopathy (OIR). Here, we utilized a genetic knock-in mouse to block atypical p38 activity (Tab1

Indexed as

MAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesRetinal DiseasesRetinal NeovascularizationRetinal VesselsAdaptor Proteins, Signal TransducingAnimalsMiceMice, Inbred C57BLOxygenRetinaSignal TransductionAdaptor Proteins, Signal TransducingOxygenp38 Mitogen-Activated Protein Kinasesangiogenesisatypical p38oxygen‐induced retinopathyretinaTab1

Identifiers

PMID41388865
PMCPMC12701566

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.