Evidence map›Paper›PMID 41751974›Full record

ArticleInternational journal of molecular sciences2026

Interleukin-17A Orchestrates Lung Injury and Remodeling Through p53 and uPA System Crosstalk.

Durgesh Nandini Das, Akarsha Balnadupete, Rashmi Shetty, Venkadesa Perumal Gopu, Rushil Sajjan, Yashodhar P Bhandary, Amarnath S Marudamuthu, Christian Oliver, Aarav Patel, Aryan Patel and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Erythromycin inhibits the differentiation of NCRJournal of thoracic disease · 2026
    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

16 authors.

Durgesh Nandini DasTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Akarsha BalnadupeteTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.ORCID 0000-0001-8850-6396
Rashmi ShettyTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.ORCID 0009-0005-1298-9498
Venkadesa Perumal GopuTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Rushil SajjanTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Yashodhar P BhandaryTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Amarnath S MarudamuthuTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.ORCID 0000-0002-3300-5743
Christian OliverTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Aarav PatelTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Aryan PatelTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Buka SamtenTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Yoichiro IwakuraResearch Institute for Biomedical Sciences, Tokyo University of Science, Chiba 278-0022, Japan.
Hua TangTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.
Deborah E CitrinRadiation Oncology Branch, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA.
Jay PetersDepartment of Medicine, Division of Pulmonary Diseases & Critical Care Medicine, The University of Texas Health Science Center at San Antonio, 4502 Medical Dr., San Antonio, TX 78229, USA.ORCID 0000-0002-5230-1062
Sreerama ShettyTexas Lung Injury Institute, Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.

Funding

National Institute of Health grants CA282561National Institute of Health grants ES025815National Institute of Health grants HL151397
6 · The paper itself

Abstract

Alveolar inflammation, elevated interleukin-17A (IL-17A), and fibrin deposition are common features in all forms of lung injury followed by fibrotic repair. Type II alveolar epithelial cell (AEC) viability, regulated by tumor suppressor protein p53 and changes in uPA-mediated fibrinolysis, has been linked to lung injury and pulmonary fibrosis (PF). Nevertheless, mechanistic details linking increased IL-17A with p53 and PAI-1 to lung injury and remodeling remain unclear. We found that IL-17A and its receptor (IL-17RA) are induced during various lung injuries. IL-17A augments IL-17RA, p53 and downstream PAI-1 with a concurrent decrease in uPA and its receptor (uPAR) in AECs. These changes promote AEC apoptosis, alveolar injury and PF. In addition, IL-17A causes a dose-dependent increase in IL-17RA and profibrogenic markers in lung fibroblasts (LFs), suggesting myofibroblast differentiation. We further found that inhibition of IL-17A by caveolin-1 scaffolding domain peptide (CSP) or its 7-mer deletion fragment (CSP7) inhibits AEC apoptosis, lung inflammation, and profibrogenic markers in LFs and PF. Further, treatment of mice with bleomycin-induced lung injury using CSP7, an anti-IL-17A antibody, or an IL-17RA blocking antibody attenuates total lung hydroxyproline and soluble collagen content, as well as levels of profibrogenic markers. These observations support the role of IL-17A/IL-17RA signaling in lung injury and post-injury remodeling.

Indexed as

Interleukin-17Lung InjuryTumor Suppressor Protein p53Alveolar Epithelial CellsAnimalsApoptosisBleomycinFibroblastsHumansMaleMiceMice, Inbred C57BLPlasminogen Activator Inhibitor 1Pulmonary FibrosisReceptors, Interleukin-17Signal TransductionBleomycinIl17ra protein, mouseInterleukin-17Plasminogen Activator Inhibitor 1Receptors, Interleukin-17Tumor Suppressor Protein p53alveolar epithelial cellsanti-IL-17A/IL-17RACSP7IL-17Alung fibrosis

Identifiers

PMID41751974
PMCPMC12940268

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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.