Evidence map›Paper›PMID 42499485›Full record

ArticleFrontiers in pharmacology2026

Proteomic results indicate inhibition of complement cascades is one of the mechanisms underlying the protective effects of Tongxinluo against myocardial infarction.

Ziqin Zhou, Ce Zhang, Yao Jiang, Yuejin Yang, Guihao Chen, Qi Pan, Jimei Chen

Abstract read
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

7 authors.

Ziqin Zhou *State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Ce Zhang *State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yao JiangState Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Yuejin YangState Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Guihao ChenState Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Qi PanState Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Jimei ChenGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Tongxinluo (TXL), a traditional Chinese medicine, has demonstrated cardioprotective effects in acute myocardial infarction (AMI), yet its impact on myocardial protein profiles remains largely unexplored. This study aimed to elucidate the proteomic mechanisms underlying the therapeutic effects of TXL in AMI. Methods: AMI was induced via left anterior descending artery ligation in C57BL/6J mice. TXL was administered by oral gavage during the acute phase. Myocardial tissues and serum were subjected to 4D label-free quantitative proteomics, Western blotting, ELISA, immunofluorescence, TUNEL staining, and molecular docking analyses. Cardiac function was evaluated by echocardiography and fibrosis was quantified by Sirius red staining. Results: Proteomic analysis identified 1,061 differentially expressed proteins between TXL- and vehicle-treated AMI mice, with KEGG enrichment highlighting significant downregulation of complement and coagulation cascades. Key complement components C1qa and C1s were markedly upregulated post-AMI but significantly suppressed by TXL. Molecular docking suggested potential interactions between multiple TXL bioactive compounds and C1qa/C1s. TXL treatment reduced complement activation (serum C3a), inhibited cardiomyocyte apoptosis (Bax/Bcl-2, TUNEL), improved left ventricular ejection fraction, and attenuated fibrosis. Notably, TXL monotherapy outperformed C1 inhibitor (C1i) alone, while combining C1i with TXL conferred no additional benefit, indicating that C1 complement inhibition is an intrinsic component of TXL's mechanism. Conclusion: Modulation of C1-associated complement activation may be one of the mechanisms through which TXL protects against AMI, providing novel proteomic-level insights into the cardioprotective actions of this traditional Chinese medicine.

Indexed as

acute myocardial infarctionC1qAcardioprotectioncomplement cascadeproteomicstongxinluo

Identifiers

PMID42499485
PMCPMC13395653

What Socratic holds

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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 Socratic graph.