Xijiaqi Formula attenuates myocardial infarction-induced chronic heart failure by inhibiting TGF-β1/Smads-mediated fibroblast activation

Sep 30, 2026

Chronic heart failure (CHF) is a common and serious outcome after myocardial infarction, yet the mechanisms driving progression from MI to CHF remain insufficiently defined. This study investigated the effects of Xijiaqi Formula (XJQ) on a rat post-MI CHF model, combining chemical profiling, echocardiographic and hemodynamic assessment, histology, and transmission electron microscopy. Transcriptomics and in vitro assays evaluated TGF-β1/Smads-driven fibroblast and myofibroblast activation and downstream extracellular matrix remodeling.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages21

Reading Time53 min

AccessFree to download

Abstract

Context and Objective

Materials and Methods

In vitro and in vivo models

Transcriptomics and mechanistic assays

Results

Conclusions

Introduction

Pharmaceutical Biology 2026, Vol. 64, No. 1, 46–66 [https://doi.org/10.1080/13880209.2025.2602234](https://doi.org/10.1080/13880209.2025.2602234) ReseaRch aRticle Xijiaqi Formula attenuates myocardial infarction-induced chronic heart failure by inhibiting TGF-β1/Smads-mediated fibroblast activation Qian Zhanga*, Jie chena*, lin-Nan Zhoub*, Xue-Fen Wua, Yu-Zhuo Wuc, Wan-ting lic, Gui-Yang Xiaa, huan Xiaa, hong-cai shanga, Xiao-hong Weia and sheng lina,b aKey laboratory of chinese internal medicine of ministry of education, Dongzhimen hospital, Beijing university of chinese medicine, Beijing, china; bPharmaceutical research center, School of chinese materia medica, Beijing university of chinese medicine, Beijing, china; cPharmaceutical research center, Second affiliated hospital, Dalian medical university, Dalian, liaoning, china ABSTRACT Context: chronic heart failure (chF) is the common concern following myocardial infarction. Xijiaqi Formula (XJQ) effectively treats chF clinically while the underlying mechanism remains unclarified. Objective: this study was designed to investigate the effect and mechanism of XJQ onchF in rats following Mi. Materials and methods: UhPlc-Q-tOF-Ms/Ms was utilized to analyze the constituents of XJQ. Post-Mi chF was induced in rats by permanent ligation of the left anterior descending coronary artery. cardiac function was assessed by echocardiogram and hemodynamic. Myocardial morphology, fibrosis, and ultrastructure were evaluated through he staining, Masson staining, and transmission electron microscopy, respectively. Myocardial transcriptomics were employed to identify genes that may be altered in response to XJQ treatment. consistently, XJQ inhibited tGF-β1-induced myofibroblast activation in vitro. Results: XJQ significantly improved cardiac function and structure, mitigating fibrosis, edema, and mitochondrial damage, while reducing key biomarkers (BNP, Nt-proBNP, ctnt, ang ii). transcriptomic analysis indicated that the differentially expressed genes influenced by XJQ were predominantly associated with extracellular matrix (ecM) remodeling. Notably, XJQ inhibited the upregulation of ecM proteins, including Adamts2, Fbln1, Itgbl1, and Ltbp3 mRNas, as well as the proteins tGF-β1, P-smad2/3, and MMP2. additionally, in vitro experiments revealed that XJQ significantly suppressed the activation of myofibroblasts induced by tGF-β1. Conclusions: XJQ significantly attenuated the progression from Mi to chF by inhibiting fibroblast activation mediated by tGF-β1/smads signaling. the molecular mechanisms underlying this effect appear to be intricately linked to its regulation of ecM remodeling proteins, specifically Adamts2, Itgbl1, Fbln1, and Ltbp3. Introduction ARTICLE HISTORY received 3 august 2025 revised 2 December 2025 accepted 5 December 2025 KEYWORDS Xijiaqi Formula; chronic heart failure; myocardial fibrosis; extracellular matrix remodeling; tgF-β1 Chronic heart failure (CHF) is the predominant outcome following a myocardial infarction (MI)(Bahit et al. 2018; Jenča et al. 2021) . Although angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers may provide some symptomatic relief for CHF that occurs post-MI, there remains a lack of effective strategies to reverse the progression from MI to CHF (Roger 2021) . The persistent high rates of morbidity and mortality associated with CHF underscore the urgent need for comprehensive approaches to address this condition. CONTACT Sheng lin [lsznn@bucm.edu.cn](lsznn@bucm.edu.cn) Key laboratory of chinese internal medicine of ministry of education and Beijing, Dongzhimen hospital affiliated to Beijing university of chinese medicine, 5 haiyuncang hutong, Dongcheng District, Beijing, 100700, china; Xiao-hong Wei [weixiaohong@bucm.edu.cn](weixiaohong@bucm.edu.cn) Key laboratory of chinese internal medicine of ministry of education and Beijing, Dongzhimen hospital affiliated to Beijing university of chi

FAQs

What is the main goal of the study on Xijiaqi Formula (XJQ)?

To determine how XJQ affects post-myocardial infarction chronic heart failure and to clarify its underlying mechanism.

How was post-MI CHF modeled and how was cardiac function evaluated?

CHF was induced in rats by permanent ligation of the left anterior descending coronary artery, and cardiac function was assessed using echocardiography and hemodynamic measurements.

What mechanism did the study identify for how XJQ attenuates CHF progression?

XJQ attenuated the MI-to-CHF progression by inhibiting TGF-β1/Smads-mediated fibroblast activation and regulating extracellular matrix (ECM) remodeling proteins such as Adamts2, Fbln1, Itgbl1, and Ltbp3.

Sep 30, 2026

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