Evidence map›Paper›PMID 42147326›Full record

ArticleFrontiers in pharmacology2026

Integrated pharmacology and experimental validation reveals potential multiple mechanisms of the neutrophil elastase inhibitor sivelestat in attenuating myocarditis.

Ruguo Ren, Ning Wang, Chen Chen, Miao Yang, Bin Li, Yuxuan Yang, Hang Zhang, Bo Yang, Yu Wu, Wei Gao and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Ruguo Ren *Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Ning Wang *Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University and Anhui Public Health Clinical Center, Hefei, Anhui, China.
Chen Chen *Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University and Anhui Public Health Clinical Center, Hefei, Anhui, China.
Miao YangCornerstone of Health Technology (Shaanxi) Co., Ltd., Xianyang, Shaanxi, China.
Bin LiDepartment of Cardiothoracic and Vascular Surgery and Critical Care Medicine, Xi'an No.1 Hospital and The First Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.
Yuxuan YangDepartment of Cardiothoracic and Vascular Surgery and Critical Care Medicine, Xi'an No.1 Hospital and The First Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.
Hang ZhangDepartment of Cardiothoracic and Vascular Surgery and Critical Care Medicine, Xi'an No.1 Hospital and The First Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.
Bo YangDepartment of Cardiothoracic and Vascular Surgery and Critical Care Medicine, Xi'an No.1 Hospital and The First Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.
Yu WuDepartment of Cardiothoracic and Vascular Surgery and Critical Care Medicine, Xi'an No.1 Hospital and The First Affiliated Hospital of Northwest University, Xi'an, Shaanxi, China.
Wei Gao *Department of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yuanyuan Hou *Department of Anesthesiology, Xi'an Chest Hospital and Northwest University Affiliated Chest Hospital, Xi'an, Shaanxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Myocarditis is an inflammatory cardiomyopathy characterized by high level of inflammatory cell infiltration and progressive cardiac dysfunction. The underlying pathogenesis involves direct pathogen damage and inflammation-mediated tissue destruction. Previous studies showed the therapeutic potential of Sivelestat (the neutrophil elastase inhibitor) in mice models, but the underlying mechanisms remain elusive. Objective: To elucidate the cardioprotective mechanisms of Sivelestat, a neutrophil elastase inhibitor, in experimental autoimmune myocarditis (EAM). Methods: Network pharmacology identified shared targets between Sivelestat and myocarditis. Molecular docking validated binding affinities. EAM was induced in male BALB/c mice (n = 6/group) using α-myosin heavy chain peptide. Interventions included Sivelestat sodium (50/100/200 mg/kg/day i. p., 14 days). Cardiac function (echocardiography), inflammation (serum IL-1β/IL-6/TNF-α/cTn; histopathology; immunohistochemistry for myocardial IL-6, IL-1β, and TNF-α), NETosis (Cit-H3/NE immunofluorescence/Western blot/SEM), apoptosis (TUNEL), and PI3K-Akt signaling (Western blot) were assessed. Results: Computational analysis identified 41 potential targets, highlighting the PI3K-Akt and IL-17 signaling pathways as top candidates. High-affinity binding was confirmed for key targets (e.g., Conclusion: Sivelestat mitigated myocarditis through multiple mechanisms, including immunomodulatory effects (NETosis inhibition and

Indexed as

Balb/c miceimmune myocarditismolecular dockingnetwork pharmacologyneutrophil extracellular traps (NETs)PI3K-Akt pathwaysivelestat

Identifiers

PMID42147326
PMCPMC13171316

What Socratic holds

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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 Socratic graph.