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March 7, 2026Frontiers in Cardiovascular Medicine2 citationsOpen Access

Advances in targeting myocardial fibrosis: integrating mechanisms and therapeutics

ZXZihui XuChina Medical UniversityYZYuyan ZhaoChina Medical University

Key Result

Current heart failure treatments including RAAS inhibitors, SGLT2 inhibitors, and other agents show indirect antifibrotic effects on myocardial fibrosis, but specific anti-fibrotic therapies are not yet established in clinical practice.

Key Points

  • The review aims to provide insights into the molecular mechanisms and therapeutic strategies for myocardial fibrosis.
  • Summarizes current knowledge on molecular pathways related to myocardial fibrosis.
  • Discusses recent advancements in experimental and analytical approaches.
  • Incorporates findings from single-cell and spatial transcriptomic studies.
  • Identifies key molecular pathways involved in myocardial fibrosis.
  • Highlights limitations of existing pharmacological interventions.
  • Discusses the heterogeneity of fibrotic signaling and its translational challenges.

PICO

P
Population
Patients with cardiovascular diseases complicated by myocardial fibrosis across diverse etiologies including hypertensive heart disease, ischemic cardiomyopathy, diabetic cardiomyopathy, and heart failure

Limitations

  • Lack of specific antifibrotic drugs routinely used clinically.
  • Existing drugs have low target specificity, uncertain long-term efficacy, and mechanisms in humans are incompletely defined.
  • High heterogeneity of myocardial fibrosis limits universal therapeutic efficacy.
  • Animal models lack full recapitulation of human chronic myocardial fibrosis.
  • Lack of robust fibrosis-specific biomarkers complicates patient stratification and therapeutic monitoring.
  • Many profibrotic pathways play essential roles in tissue repair, raising concerns about off-target effects and safety of direct inhibitors.
  • Myocardial fibrosis is highly heterogeneous with respect to etiology, disease stage, and spatial distribution, limiting the effectiveness of uniform treatment strategies.
  • Commonly used animal models fail to fully recapitulate the chronic, multifactorial nature of human cardiac fibrosis.
  • Lack of robust, fibrosis-specific biomarkers complicates patient stratification and therapeutic monitoring.
  • Many profibrotic pathways play essential roles in tissue repair and homeostasis, raising concerns regarding target specificity and off-target effects.

Abstract

Myocardial fibrosis (MF) is a maladaptive pathological response of the heart to chronic injury. Accumulating evidence indicates that MF plays a central role in the development and progression of hypertensive heart disease, ischemic cardiomyopathy, diabetic cardiomyopathy, and heart failure, and is closely associated with an increased risk of arrhythmias and sudden cardiac death. In recent years, advances in experimental and analytical approaches have improved our understanding of the molecular mechanisms underlying MF and informed the development of potential therapeutic strategies. However, many existing pharmacological interventions exhibit limited target specificity, uncertain long-term efficacy, and incompletely defined mechanisms of action in humans. In this review, we summarize the major molecular pathways involved in myocardial fibrosis and discuss current and emerging therapeutic approaches, incorporating mechanistic insights from recent single-cell and spatial transcriptomic studies to better contextualize fibrotic signaling heterogeneity and translational challenges.

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Cite This Study

Xu et al. (2026) conducted a review in Patients with cardiovascular diseases complicated by myocardial fibrosis across diverse etiologies including hypertensive heart disease, ischemic cardiomyopathy, diabetic cardiomyopathy, and heart failure. Current heart failure treatments including RAAS inhibitors, SGLT2 inhibitors, and other agents show indirect antifibrotic effects on myocardial fibrosis, but specific anti-fibrotic therapies are not yet established in clinical practice.

synapsesocial.com/papers/69abc1015af8044f7a4e994ehttps://doi.org/10.3389/fcvm.2026.1769016
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