About this Research Topic
Vascular remodeling is a process characterized by the dysregulation of migration, proliferation, and apoptosis of vascular cells, leading to the thickening or thinning of the vessel wall. This process is a key factor in the development of various cardiovascular diseases, such as hypertension, atherosclerosis, pulmonary artery hypertension, and restenosis. Accumulating evidence suggests that altered vascular smooth muscle cells (VSMCs) proliferation, migration, differentiation, inflammation, calcification, oxidative stress, apoptosis, and phenotype switching play an important role in regulating the development and progression of vascular remodeling. Therefore, clarifying the molecular mechanisms of VSMCs in vascular remodeling and targeting this process has emerged as a promising strategy for the prevention and treatment of cardiovascular diseases.
Given the significant impact of vascular remodeling on cardiovascular diseases, understanding its pathophysiology is a major priority for cardiovascular research. In this research topic, we aim to focus on the cellular and pathophysiological mechanisms, and prevention strategies of the dysfunction of VSMCs in vascular remodeling. It will provide a comprehensive discussion of the pathophysiologic basis of VSMC phenotype switching, inflammation, hyperproliferation, migration of VSMCs, vascular calcification, and synthesis of the extracellular matrix of VSMCs.
We welcome submissions on the following topics, but are not limited to:
- Smooth muscle cell differentiation and phenotypic switching
- Oxidative stress, apoptosis, and senescence in VSMCs dysfunction
- Autophagy, pyroptosis, and ferroptosis of VSMCs in vascular remodeling
- Inflammation signaling and immune response of VSMCs in vascular remodeling
- Mitochondrial dysfunction of VSMCs in vascular remodeling
- VSMCs and vascular calcification
- Interaction between VSMCs and endothelial cells or fibroblast in vascular remodeling
- The drug and non-drug treatment for vascular remodeling
Given the significant impact of vascular remodeling on cardiovascular diseases, understanding its pathophysiology is a major priority for cardiovascular research. In this research topic, we aim to focus on the cellular and pathophysiological mechanisms, and prevention strategies of the dysfunction of VSMCs in vascular remodeling. It will provide a comprehensive discussion of the pathophysiologic basis of VSMC phenotype switching, inflammation, hyperproliferation, migration of VSMCs, vascular calcification, and synthesis of the extracellular matrix of VSMCs.
We welcome submissions on the following topics, but are not limited to:
- Smooth muscle cell differentiation and phenotypic switching
- Oxidative stress, apoptosis, and senescence in VSMCs dysfunction
- Autophagy, pyroptosis, and ferroptosis of VSMCs in vascular remodeling
- Inflammation signaling and immune response of VSMCs in vascular remodeling
- Mitochondrial dysfunction of VSMCs in vascular remodeling
- VSMCs and vascular calcification
- Interaction between VSMCs and endothelial cells or fibroblast in vascular remodeling
- The drug and non-drug treatment for vascular remodeling
Keywords: vascular smooth muscle cells, vascular remodeling, hypertension, atherosclerosis, restenosis
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.
