About this Research Topic
This Research Topic is part of a series with:
Vascular Smooth Muscle Cell fate and Vascular Remodeling: Mechanisms, Therapeutic Targets, and Drugs, Volume II
Vascular smooth muscle cells (VSMCs) are required for organ functioning in the development and physiology of the circulation system. VSMCs have emerged as pivotal players in the pathogenesis of various cardiovascular diseases, including atherosclerosis, aneurysm, hypertension, vascular calcification, and arterial stiffness. VSMCs generally demonstrate unique phenotype, molecular and functional features. However, under pathological state, VSMCs cell fate and state changes as phenotypic modulation/plasticity or dedifferentiation into individual fibroblast-like, macrophage-like, or osteoblast-like cells. Furthermore, VSMC fate alteration leads to the structure altering and arrangement of blood vessels, called vascular remodeling, contributing to cardiovascular disease progression. There is currently no effective therapy to block the VSMC phenotypic switch and vascular remodeling. Therefore, improving our understanding of the cellular and molecular basis of VSMC fate change will help develop strategic therapeutic targets and effective medicines for cardiovascular diseases.
VSMCs fate has been associated with intrinsic developmental programs and epigenetic pathways and signals from the microenvironment, including cell-cell communications and VSMC-extracellular matrix interactions. However, studies on the molecular processes of VSMCs fidelity are not fully elucidated. VSMCs may have spatiotemporal genetic or epigenetic markers, depending on the tissue where they reside and the niche to which they are linked. Although VSMCs show distinct molecular and phenotypic features under physiological and pathological conditions, they are heterogeneous and plastic in different vascular beds and tissues. Hence, it is crucial to understand the molecular mechanisms underlying VSMC fate regulation involved in cardiovascular diseases and tissue regeneration, emerging novel therapeutic targets and medicines to regulate VSMC fate and vascular remodeling for the prevention of cardiovascular disease progression.
This Research Topic will showcase advances in both biomedical and pharmacological studies of vascular smooth muscle cell biology, arteriogenesis, vascular remodeling, aging, and the vascular niche under physiological and pathological conditions. We welcome original research articles, clinical case report, reviews, and short communications, falling under, but not limited to, the following areas:
• Pharmacology of VSMC plasticity in health and disease;
• Molecular mechanisms of VSMC fate regulation including proliferation, migration, apoptosis, quiescence, senescence, and trans-differentiation;
• Molecular mechanism underlying vascular formation and function;
• The role of VSMC fate regulation in the pathogenesis of the cardiovascular diseases;
• Therapeutic effects of clinical medicine and natural products on VSMC function and cell fate for treatment of cardiovascular diseases.
Vascular Smooth Muscle Cell fate and Vascular Remodeling: Mechanisms, Therapeutic Targets, and Drugs, Volume II
Vascular smooth muscle cells (VSMCs) are required for organ functioning in the development and physiology of the circulation system. VSMCs have emerged as pivotal players in the pathogenesis of various cardiovascular diseases, including atherosclerosis, aneurysm, hypertension, vascular calcification, and arterial stiffness. VSMCs generally demonstrate unique phenotype, molecular and functional features. However, under pathological state, VSMCs cell fate and state changes as phenotypic modulation/plasticity or dedifferentiation into individual fibroblast-like, macrophage-like, or osteoblast-like cells. Furthermore, VSMC fate alteration leads to the structure altering and arrangement of blood vessels, called vascular remodeling, contributing to cardiovascular disease progression. There is currently no effective therapy to block the VSMC phenotypic switch and vascular remodeling. Therefore, improving our understanding of the cellular and molecular basis of VSMC fate change will help develop strategic therapeutic targets and effective medicines for cardiovascular diseases.
VSMCs fate has been associated with intrinsic developmental programs and epigenetic pathways and signals from the microenvironment, including cell-cell communications and VSMC-extracellular matrix interactions. However, studies on the molecular processes of VSMCs fidelity are not fully elucidated. VSMCs may have spatiotemporal genetic or epigenetic markers, depending on the tissue where they reside and the niche to which they are linked. Although VSMCs show distinct molecular and phenotypic features under physiological and pathological conditions, they are heterogeneous and plastic in different vascular beds and tissues. Hence, it is crucial to understand the molecular mechanisms underlying VSMC fate regulation involved in cardiovascular diseases and tissue regeneration, emerging novel therapeutic targets and medicines to regulate VSMC fate and vascular remodeling for the prevention of cardiovascular disease progression.
This Research Topic will showcase advances in both biomedical and pharmacological studies of vascular smooth muscle cell biology, arteriogenesis, vascular remodeling, aging, and the vascular niche under physiological and pathological conditions. We welcome original research articles, clinical case report, reviews, and short communications, falling under, but not limited to, the following areas:
• Pharmacology of VSMC plasticity in health and disease;
• Molecular mechanisms of VSMC fate regulation including proliferation, migration, apoptosis, quiescence, senescence, and trans-differentiation;
• Molecular mechanism underlying vascular formation and function;
• The role of VSMC fate regulation in the pathogenesis of the cardiovascular diseases;
• Therapeutic effects of clinical medicine and natural products on VSMC function and cell fate for treatment of cardiovascular diseases.
Keywords: Smooth muscle cells, Transdifferentiation, Reprogramming, Therapeutic targets, Cardiovascular diseases
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
