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Cellular and Molecular Mechanisms of Cardiovascular Repair

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 25 February 2026 | Viewed by 4722

Special Issue Editor

Special Issue Information

Dear Colleagues,

We are delighted to introduce this  Special Issue of IJMS which explores the intricate processes governing cardiovascular repair and regeneration. This collection aims at highlighting the key roles of defence and repair cell types, such as immune cells and fibroblasts, in injury mending, emphasizing their contribution to cardiac scar formation and remodeling, as well as other accessory mechanisms such as new vessel formation. Furthermore, we will try to provide novel insights into the dynamics of the extracellular matrix (ECM) within physiopathological conditions and elucidate its critical function in supporting tissue structure and inter-cellular communication during fibrosis and healing. Additionally, this Special Issue aims at exploring the mechanisms of fibrosis and its intertwined relationship with inflammation, offering a comprehensive understanding of its impact on cardiovascular function post-injury. We seek contributions also examining angiogenesis, as a vital process in restoring oxygen supply and promoting tissue recovery. By integrating all these key aspects, our collection will provide a holistic view of cardiovascular repair, aiming to advance physiopathology comprehension, as well as suggesting novel therapeutic strategies for cardiovascular diseases. We aim to attract the attention of both researchers and clinicians dedicated to translational cardiovascular reseach and advancing cardiovascular medicine.

Suitable topics include, but are not limited to, the following:

  • Role of different cell types in cardiovascular repair mechanisms;
  • Interplay between inflammation and fibrosis;
  • Mechanisms of cardio-protection;
  • Angiogenesis in cardiovascular repair;
  • Novel therapeutic targets or strategies.

Dr. Isotta Chimenti
Guest Editor

Manuscript Submission Information

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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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • fibroblasts
  • injury repair
  • cardiac scar
  • extracellular matrix
  • fibrosis
  • angiogenesis
  • inflammation
  • cardioprotection

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Published Papers (3 papers)

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Review

67 pages, 7370 KB  
Review
Molecular and Cellular Effects of Microplastics and Nanoplastics in the Pathogenesis of Cardiovascular, Nervous, Urinary, Digestive, and Reproductive System Diseases: A Global Systematic Review
by Vasilii Chulkov, Mitkhat Gasanov, Vladimir Isakov, Anastasia Denisenko, Chizaram Nwosu and Stanislav Rodkin
Int. J. Mol. Sci. 2025, 26(22), 11194; https://doi.org/10.3390/ijms262211194 - 19 Nov 2025
Viewed by 866
Abstract
Microplastics (MPs) and nanoplastics (NPs), formed as a result of plastic product degradation, pose a global environmental threat by penetrating biological systems and inducing systemic pathological changes. This systematic review, conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses [...] Read more.
Microplastics (MPs) and nanoplastics (NPs), formed as a result of plastic product degradation, pose a global environmental threat by penetrating biological systems and inducing systemic pathological changes. This systematic review, conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews guidelines, aims to analyze the molecular and cellular mechanisms of the toxic effects of MPs and NPs on the human cardiovascular, nervous, reproductive, urinary, and digestive systems. The primary mechanisms include oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, autophagy, ferroptosis, and impaired barrier functions. In the cardiovascular system, MPs and NPs contribute to endothelial dysfunction, disorders of lipid metabolism, and fibrosis; in the nervous system, they promote neuroinflammation, pathological protein aggregation, and psychiatric disorders; in the reproductive system, they lead to hormonal imbalance and reduced fertility; in the kidneys, they cause inflammation, and fibrosis and lead to deterioration of kidney function; and in the gastrointestinal tract, they contribute to dysbiosis and metabolic disorders. The literature search was conducted in the PubMed, Web of Science, and Scopus databases without limitations on date, language, or access. Studies were selected based on criteria of transparency, statistical validity, sample representativeness, and correctness of data interpretation. The review emphasizes the necessity of an interdisciplinary approach to developing prevention and treatment strategies, including reduction in exposure, antioxidant and immunomodulatory therapy, and restoration of barrier functions and microbiota. The data obtained reveal research gaps and identify directions for further study. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular Repair)
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30 pages, 2635 KB  
Review
Monocytes/Macrophages and Atherogenesis
by Sergey Kozlov, Tatiana Riazantseva, Ivan Melnikov, Sergey Okhota, Viktoriia Vasenkova, Olga Saburova, Yuliya Avtaeva, Konstantin Guria, Lyudmila Prokofieva and Zufar Gabbasov
Int. J. Mol. Sci. 2025, 26(22), 10962; https://doi.org/10.3390/ijms262210962 - 12 Nov 2025
Viewed by 525
Abstract
Atherosclerosis is a widespread cardiovascular disease characterized by retention of atherogenic lipoproteins in the arterial wall and the onset of subclinical vascular inflammation; the development of atherosclerotic plaques; eventual narrowing of the arterial lumen and/or plaque disruption; and subsequent manifestation with stable ischemia [...] Read more.
Atherosclerosis is a widespread cardiovascular disease characterized by retention of atherogenic lipoproteins in the arterial wall and the onset of subclinical vascular inflammation; the development of atherosclerotic plaques; eventual narrowing of the arterial lumen and/or plaque disruption; and subsequent manifestation with stable ischemia or acute atherothrombotic events. Numerous cell types are implicated in atherogenesis. Monocytes/macrophages are considered pivotal participants in this complex process. They play a crucial role in the onset and augmentation of inflammation and greatly contribute to atherosclerotic plaque growth and destabilization. However, monocytes/macrophages are also essential for the resolution of inflammation and the stabilization of atherosclerotic lesions. In this regard, studies of the function of monocytes/macrophages in relation to this disease are of considerable interest to researchers, as the results can help to design new drugs aimed at preventing the development of atherosclerosis and its complications. This review presents current data on the classification and functions of monocytes/macrophages; discusses current hypotheses regarding the involvement of monocytes/macrophages in atherogenesis; and highlights existing gaps in evidence. This review is primarily aimed at readers with a background in clinical medicine who are interested in the involvement of monocytes/macrophages in atherogenesis. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular Repair)
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14 pages, 816 KB  
Review
The Role of Cardiac Fibroblast Heterogeneity in Myocardial Fibrosis and Its Novel Therapeutic Potential
by Isotta Chimenti, Francesca Pagano, Claudia Cozzolino, Francesca Icolaro, Erica Floris and Vittorio Picchio
Int. J. Mol. Sci. 2025, 26(12), 5882; https://doi.org/10.3390/ijms26125882 - 19 Jun 2025
Cited by 4 | Viewed by 2804
Abstract
Cardiac fibrosis is a key physiopathological process underlying the progression of virtually all heart diseases and related conditions, including myocardial infarction, pressure overload, and heart failure. Once regarded as a homogeneous and passive population, cardiac fibroblasts are now recognized as highly heterogeneous and [...] Read more.
Cardiac fibrosis is a key physiopathological process underlying the progression of virtually all heart diseases and related conditions, including myocardial infarction, pressure overload, and heart failure. Once regarded as a homogeneous and passive population, cardiac fibroblasts are now recognized as highly heterogeneous and dynamic, comprising distinct subpopulations with specialized molecular and functional identities. These subpopulations include resident fibroblasts, activated myofibroblasts, matrifibrocytes, inflammatory fibroblasts, and senescent fibroblasts, each contributing uniquely to extracellular matrix (ECM) remodeling, cytokine secretion, and intercellular crosstalk. Recent advances in single-cell transcriptomics, lineage tracing, and epigenetic profiling have revealed the plasticity and phenotypic transitions of cardiac fibroblasts in both physiological and pathological contexts. This review synthesizes current knowledge on fibroblast diversity in the adult heart, including their embryological origins and anatomical distribution, and explores how these insights could guide the development of precision anti-fibrotic therapies. We discuss a selection of emerging therapeutic strategies, including subtype-specific targeting (e.g., anti-POSTN, anti-IL1β), modulation of key signaling pathways (e.g., TGF-β, Wnt, Notch), with a brief mention also of novel approaches based on non-coding RNAs and epigenetic regulators. A better understanding of cardiac fibroblast heterogeneity holds significant potential for the design of more specific cell-type and context-tailored interventions, moving toward more effective and personalized treatments for cardiac fibrosis and its sequelae. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Cardiovascular Repair)
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