Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway

BackgroundWhile platelet hyperreactivity constitutes an independent risk factor for major adverse cardiovascular events (MACEs) in coronary artery disease, its molecular underpinnings remain poorly characterized. Recent advances in transcriptomic profiling have revealed potential associations with s...

Full description

Saved in:
Bibliographic Details
Main Authors: Shengnan Shi, Jiaming Gao, Yehao Zhang, Min Zhan, Zhanfei Tan, Peili Wang, Jianhua Fu, Jianxun Liu
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-03-01
Series:Frontiers in Pharmacology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2025.1535182/full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849343686612090880
author Shengnan Shi
Jiaming Gao
Yehao Zhang
Min Zhan
Zhanfei Tan
Peili Wang
Jianhua Fu
Jianxun Liu
author_facet Shengnan Shi
Jiaming Gao
Yehao Zhang
Min Zhan
Zhanfei Tan
Peili Wang
Jianhua Fu
Jianxun Liu
author_sort Shengnan Shi
collection DOAJ
description BackgroundWhile platelet hyperreactivity constitutes an independent risk factor for major adverse cardiovascular events (MACEs) in coronary artery disease, its molecular underpinnings remain poorly characterized. Recent advances in transcriptomic profiling have revealed potential associations with specific RNA signatures. Through systematic bioinformatics analysis of differential gene expression patterns and pathway activation in CHD patients, this study aims to elucidate key molecular regulators of platelet hyperactivity, establishing a theoretical framework for developing precision therapeutic strategies to mitigate post-CHD complications.MethodsThis randomized controlled study included 16 CHD patients and 16 healthy controls. Inflammation markers, platelet aggregation function, and CD62p levels were assessed using flow cytometry. Mitochondrial morphology and organelles were observed using scanning electron microscopy and transmission electron microscopy. Genes related to symptom alteration between CHD patients and healthy controls were identified using the criteria of p < 0.05. The molecular correlations of these genes were analyzed using a comprehensive perspective that included Gene Ontology (GO) biological process and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Western blot and correlation analyses were also conducted to validate the expression and diagnostic value of the DEGs.ResultsCHD patients exhibited alterations in platelet organelles ultrastructure, heightened platelet activation and aggregation, and disturbance of the inflammatory equilibrium. RNA sequencing demonstrated distinct changes in the gene expression profiles of circulating platelets from CHD patients. The increase in platelet activation and aggregation could be partially associated with the upregulation of the Talin-1 and αIIbβ3 proteins expression.ConclusionAbnormal transcription and platelet activation occur after CHD onset, and upregulation of the Talin-1/αIIbβ3-mediated bidirectional signaling pathway are the primary pathological features.Clinical Trial Registrationhttps://www.chictr.org.cn/, identifier ChiCTR2100041998.
format Article
id doaj-art-eec7d21eb98c4e96915052b986f83d49
institution Kabale University
issn 1663-9812
language English
publishDate 2025-03-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Pharmacology
spelling doaj-art-eec7d21eb98c4e96915052b986f83d492025-08-20T03:42:53ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-03-011610.3389/fphar.2025.15351821535182Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathwayShengnan Shi0Jiaming Gao1Yehao Zhang2Min Zhan3Zhanfei Tan4Peili Wang5Jianhua Fu6Jianxun Liu7Beijing Key Laboratory of Pharmacology of Chinese Materia Medica, Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBeijing Key Laboratory of Pharmacology of Chinese Materia Medica, Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBeijing Key Laboratory of Pharmacology of Chinese Materia Medica, Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaDepartment of Encephalopathy, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaWangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaNational Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBeijing Key Laboratory of Pharmacology of Chinese Materia Medica, Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBeijing Key Laboratory of Pharmacology of Chinese Materia Medica, Institute of Basic Medical Sciences of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBackgroundWhile platelet hyperreactivity constitutes an independent risk factor for major adverse cardiovascular events (MACEs) in coronary artery disease, its molecular underpinnings remain poorly characterized. Recent advances in transcriptomic profiling have revealed potential associations with specific RNA signatures. Through systematic bioinformatics analysis of differential gene expression patterns and pathway activation in CHD patients, this study aims to elucidate key molecular regulators of platelet hyperactivity, establishing a theoretical framework for developing precision therapeutic strategies to mitigate post-CHD complications.MethodsThis randomized controlled study included 16 CHD patients and 16 healthy controls. Inflammation markers, platelet aggregation function, and CD62p levels were assessed using flow cytometry. Mitochondrial morphology and organelles were observed using scanning electron microscopy and transmission electron microscopy. Genes related to symptom alteration between CHD patients and healthy controls were identified using the criteria of p < 0.05. The molecular correlations of these genes were analyzed using a comprehensive perspective that included Gene Ontology (GO) biological process and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Western blot and correlation analyses were also conducted to validate the expression and diagnostic value of the DEGs.ResultsCHD patients exhibited alterations in platelet organelles ultrastructure, heightened platelet activation and aggregation, and disturbance of the inflammatory equilibrium. RNA sequencing demonstrated distinct changes in the gene expression profiles of circulating platelets from CHD patients. The increase in platelet activation and aggregation could be partially associated with the upregulation of the Talin-1 and αIIbβ3 proteins expression.ConclusionAbnormal transcription and platelet activation occur after CHD onset, and upregulation of the Talin-1/αIIbβ3-mediated bidirectional signaling pathway are the primary pathological features.Clinical Trial Registrationhttps://www.chictr.org.cn/, identifier ChiCTR2100041998.https://www.frontiersin.org/articles/10.3389/fphar.2025.1535182/fullcoronary heart diseaseplatelet hyperreactivityTalin-1 and αIIbβ3-mediated bidirectional signaling pathwayplatelet transcriptomeinterleukin
spellingShingle Shengnan Shi
Jiaming Gao
Yehao Zhang
Min Zhan
Zhanfei Tan
Peili Wang
Jianhua Fu
Jianxun Liu
Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway
Frontiers in Pharmacology
coronary heart disease
platelet hyperreactivity
Talin-1 and αIIbβ3-mediated bidirectional signaling pathway
platelet transcriptome
interleukin
title Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway
title_full Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway
title_fullStr Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway
title_full_unstemmed Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway
title_short Inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of Talin-1/αIIbβ3-mediated bidirectional signaling pathway
title_sort inflammation and platelet hyperresponsiveness in coronary artery disease and the influence of talin 1 αiibβ3 mediated bidirectional signaling pathway
topic coronary heart disease
platelet hyperreactivity
Talin-1 and αIIbβ3-mediated bidirectional signaling pathway
platelet transcriptome
interleukin
url https://www.frontiersin.org/articles/10.3389/fphar.2025.1535182/full
work_keys_str_mv AT shengnanshi inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT jiaminggao inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT yehaozhang inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT minzhan inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT zhanfeitan inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT peiliwang inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT jianhuafu inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway
AT jianxunliu inflammationandplatelethyperresponsivenessincoronaryarterydiseaseandtheinfluenceoftalin1aiibb3mediatedbidirectionalsignalingpathway