Signalling Mechanisms Regulating Cardiac Fibroblast Function

A Special Issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 October 2026 | Viewed by 3047

Editors


E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA
Interests: cardiac reprogramming; epigenetics; reprogramming; molecular biology; single-cell

E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599, USA
Interests: cardiac fibrosis; scRNA-seq; cell-to-cell communication; heart regeneration

Special Issue Information

Dear Colleagues,

Cardiac fibroblasts represent a major cell population in the heart, playing essential roles in extracellular matrix (ECM) remodeling, intercellular communication, and tissue repair. In healthy myocardium, fibroblasts maintain homeostasis through balanced ECM turnover and paracrine signaling. However, under stress or injury, these cells undergo activation into myofibroblasts, leading to excessive ECM deposition, fibrosis, and impaired cardiac function. Understanding the signaling pathways that govern fibroblast behavior is therefore essential for uncovering mechanisms of both physiological adaptation and pathological remodeling.

This Special Issue will focus on the signaling mechanisms that control cardiac fibroblast activation, communication, and function across health, injury, and repair. We particularly welcome contributions that dissect intracellular pathways (e.g., TGF-β/SMAD, MAPK, PI3K-AKT, Hippo-YAP, Wnt) and their integration with extracellular and mechanical cues. Manuscripts highlighting fibroblast heterogeneity, single-cell and spatial insights, cross-talk with cardiomyocytes, endothelial cells, and immune cells, as well as novel therapeutic strategies to target fibroblast signaling, are strongly encouraged.

We invite original research articles and reviews that bring together emerging insights into the molecular and cellular mechanisms regulating cardiac fibroblast function. By consolidating these emerging insights, this Special Issue aims to provide a comprehensive resource on how fibroblast signaling contributes to cardiac pathology and to highlight new opportunities for therapeutic intervention in cardiovascular disease.

Dr. Haofei Wang
Dr. Yanhan Dong
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiac fibroblasts
  • myofibroblast activation
  • extracellular matrix remodeling
  • fibrosis
  • intercellular communication
  • mechanotransduction
  • single-cell and spatial insights
  • regeneration
  • therapeutic targeting

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

23 pages, 2668 KB  
Review
Targeting Cardiac Fibroblast Plasticity for Antifibrotic and Regenerative Therapy in Heart Failure
by Suchandrima Dutta, Sophie Chen, Waqas Ahmad, Wei Huang, Jialiang Liang and Yigang Wang
Cells 2026, 15(2), 112; https://doi.org/10.3390/cells15020112 - 8 Jan 2026
Cited by 3 | Viewed by 2579
Abstract
Cardiac fibrosis is a major component of heart failure (HF) and develops when reparative wound healing becomes chronic, leading to excessive extracellular matrix accumulation. Cardiac fibroblasts (CFs), the main regulators of matrix remodeling, are heterogeneous in developmental origins, regional localizations, and activation states. [...] Read more.
Cardiac fibrosis is a major component of heart failure (HF) and develops when reparative wound healing becomes chronic, leading to excessive extracellular matrix accumulation. Cardiac fibroblasts (CFs), the main regulators of matrix remodeling, are heterogeneous in developmental origins, regional localizations, and activation states. This diversity determines whether tissue repair resolves normally or progresses into maladaptive scarring that disrupts myocardial structure and function after injuries. Recent single-cell and spatial transcriptomic studies show that CFs exist in distinct yet interrelated molecular states in murine models and human cardiac tissue with specialized roles in matrix production, angiogenesis, immune signaling, and mechanical sensing. These insights redefine cardiac fibrosis as a dynamic and context-dependent process rather than a uniform cellular response. Although CFs are promising targets for preventing HF progression and enhancing cardiac remodeling, translation into effective therapies remains limited by the unclear heterogeneity of pathological fibroblasts, the lack of distinctive CF markers, and the broad activity of fibrogenic signaling pathways. In this review, we discuss the dynamics of CF activations during the development and progression of HF and assess the underlying pathways and mechanisms contributing to cardiac dysfunction. Additionally, we highlight the potential of targeting CFs for developing therapeutic strategies. These include nonspecific suppression of fibroblast activity and targeted modulation of the signaling pathways and cell populations that sustain chronic remodeling. Furthermore, we assess regenerative approaches that can reprogram fibroblasts or modulate their paracrine functions to restore functional myocardium. Integrating antifibrotic and regenerative strategies with advances in precision drug discovery and gene delivery offers a path toward reversing established fibrosis and achieving recovery in HF. Full article
(This article belongs to the Special Issue Signalling Mechanisms Regulating Cardiac Fibroblast Function)
Show Figures

Graphical abstract

Back to TopTop