Vascular Inflammation and Smooth Muscle Cell Dysfunction in Cardiovascular Disease

Chronic vascular inflammation and smooth muscle cell (SMC) dysfunction are central drivers in the initiation and progression of a wide range of cardiovascular diseases, including atherosclerosis, thoracic and abdominal aortic aneurysms, and aortic dissection. Recent studies have revealed that SMCs exhibit remarkable plasticity, transitioning between contractile, synthetic, and inflammatory phenotypes in response to various biochemical and biomechanical stimuli. This phenotypic switching, along with endothelial-to-mesenchymal transition (EndMT), increased vascular permeability, and extracellular matrix degradation, contributes significantly to pathological vascular remodeling.

Key molecular pathways such as those involving KLF4, noncoding RNAs (including lncRNAs), VE-cadherin, platelet-activating factor, and PKC signaling have emerged as critical regulators of vascular homeostasis and inflammation. Understanding the cellular and molecular mechanisms driving SMC dysfunction and vascular inflammation holds immense potential for identifying novel therapeutic targets and pharmacological interventions.

This Research Topic invites original research, reviews, and translational studies exploring the mechanisms, biomarkers, and therapeutic modulation of vascular inflammation and SMC dysfunction. Studies investigating the pharmacological impact of targeting inflammatory pathways, vascular remodeling processes, and SMC plasticity in preclinical and clinical settings are particularly welcome. Contributions that explore systems biology approaches, emerging drug targets, or the role of the immune system in vascular pathologies are also encouraged.

Topics of interest include, but are not limited to:
• Mechanisms of SMC phenotypic switching in vascular disease
• Endothelial-to-mesenchymal transition (EndMT) in vascular remodeling
• Regulation of vascular permeability and inflammation
• Role of KLF4, VE-cadherin, and noncoding RNAs in SMC and endothelial function
• Pharmacological modulation of vascular inflammation
• Pathophysiology of aortic aneurysm and dissection
• Immune cell-SMC cross-talk in vascular pathology
• Novel anti-inflammatory or remodeling-targeting drug candidates

We aim to highlight innovative pharmacological strategies and mechanistic insights that advance our understanding and treatment of vascular inflammatory diseases.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Technology and Code

Keywords: vascular inflammation, smooth muscle cells, atherosclerosis, endothelial dysfunction, vascular remodeling, cytokines, oxidative stress, plaque stability, immune signaling, cardiovascular disease

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.