Evidence map›Paper›PMID 41833107›Full record

ArticleRedox biology2026

Deletion of STIM1 in Treg cells protects against lung fibrosis and associated cardiovascular complications in a pre-clinical mouse model.

Nagaraja Nagre, Balaji Srinivas, Nicholas Richards, Ryan Washington, Gregory Nicholson, Yan Sanders, Beata Kosmider, Khalid Matrougui

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2026. 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. 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

8 authors.

Nagaraja NagreDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA. Electronic address: nagren@odu.edu.
Balaji SrinivasDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA.
Nicholas RichardsDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA.
Ryan WashingtonDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA.
Gregory NicholsonDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA.
Yan SandersDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA.
Beata KosmiderDepartment of Microbiology, Immunology, and Inflammation, Center for Inflammation and Lung Research, Temple University, Philadelphia, 19140, PA.
Khalid MatrouguiDepartment of Biomedical and Translational Sciences, Macon & Joan Brock Virginia Health Sciences at Old Dominion University, P.O. Box 1980, Norfolk, VA, 23501-1980, USA. Electronic address: matrouk@odu.edu.

Funding

Interleukin 12 disruption provides beta cell and microvessel protection in type 2diabetesR01HL150014 · NHLBI · OLD DOMINION UNIVERSITY · PI MATROUGUI, KHALID · 2020 to 2023
$1.8M
Stromal interaction molecule 1, immune cells, and vascular pathology in established hypertensionR01HL151616 · NHLBI · OLD DOMINION UNIVERSITY · PI MATROUGUI, KHALID · 2020 to 2023
$1.5M
Cannabinoid-2 receptor signaling in vesicant induced lung injuryR21ES033007 · NIEHS · EASTERN VIRGINIA MEDICAL SCHOOL · PI NAGRE, NAGARAJA · 2021 to 2022
$433k
NHLBI NIH HHS R01 HL150014NHLBI NIH HHS R01 HL151616NIEHS NIH HHS R21 ES033007
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and incurable lung disease characterized by excessive tissue remodeling and impaired gas exchange. Evidence highlights the critical interplay between immune regulation, calcium signaling, and redox biology implications in the pathogenesis of fibrotic lung disease. Regulatory T-cells (Tregs), known to modulate cardiovascular and immune function, are diminished in IPF, contributing to inflammation and tissue damage. Here, we demonstrate that the stromal interaction molecule 1 (STIM1), a key regulator of intracellular calcium homeostasis, is significantly upregulated in Treg cells isolated from IPF patients and mice subjected to bleomycin-induced lung injury. This upregulation is associated with increased Treg cell apoptosis, reduced Foxp3 expression, and exacerbation of pulmonary fibrosis and cardiac remodeling. Using Treg-specific STIM1 knockout mice (Treg

Indexed as

Cardiovascular DiseasesPulmonary FibrosisStromal Interaction Molecule 1T-Lymphocytes, RegulatoryAnimalsApoptosisBleomycinDisease Models, AnimalGene DeletionHumansMiceMice, KnockoutNitric OxideNitric Oxide Synthase Type IIIBleomycinNitric OxideNitric Oxide Synthase Type IIIStim1 protein, mouseStromal Interaction Molecule 1ApoptosisBleomycinCardiac fibrosisFOXp3IPFLung fibrosisPulmonary vascular endothelial functionSTIM1Treg cells

Identifiers

PMID41833107
PMCPMC13000719

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Registered trials

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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.