Unraveling the Mechanisms of Atherosclerosis: From Molecular Pathways to Clinical Outcomes

Atherosclerosis is a complex disorder that develops over many years. It begins with subtle changes in the vascular wall and progresses into a condition that affects many organs. The disease remains a leading cause of heart attack, stroke, and peripheral vascular problems. Understanding the molecular and cellular events that drive this process is essential for improving prevention and treatment.

The earliest stages of atherosclerosis involve injury to the endothelium. This injury alters the normal barrier between blood and tissue. Once the barrier becomes disrupted, lipids move into the arterial wall. Immune cells then enter this environment and create local inflammation. This inflammatory response supports the formation of fatty streaks, which are early signs of plaque development. These events reflect a failure of normal repair pathways and show the importance of vascular homeostasis.

Smooth muscle cells also play a central part in plaque formation. These cells migrate from the deeper layer of the vessel into the inner layer. Once they arrive, they begin to proliferate. They also produce extracellular matrix components that shape the plaque. Changes in smooth muscle cell behavior reflect molecular alterations in growth factor activity, oxidative stress, and metabolic imbalance.

As plaques mature, the inflammatory response becomes more complex. Macrophages accumulate and transform into foam cells. These foam cells release signals that influence collagen stability and lipid composition within the plaque. Plaques that contain unstable lipid rich cores are more likely to rupture. A ruptured plaque can lead to clot formation and block blood flow, which may cause acute and life threatening clinical events.

Recent research highlights the role of genetic variation, epigenetic change, and metabolic stress in shaping individual risk. These factors influence lipid handling, immune activation, and endothelial response to injury. They also help explain why some individuals develop severe disease while others remain protected.

Better understanding of these events supports the development of targeted therapies. These therapies aim to reduce inflammation, stabilize plaques, improve endothelial function, and correct metabolic imbalance. Clinical studies now explore how molecular pathways relate to measurable outcomes in patients.

We welcome original research, systematic reviews, meta analyses, clinical case studies, and mini reviews within the scope of this Research Topic.

Submissions may include but not limited to

• Endothelial injury and early vascular dysfunction

• Lipid accumulation and foam cell formation

• Smooth muscle cell migration and plaque remodeling

• Immune cell signaling during plaque progression

• Genetic and epigenetic factors that influence disease risk

• Molecular predictors of plaque instability and rupture

• Therapeutic strategies that improve clinical outcomes

Article types and fees

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

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

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Article types

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

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

Keywords: Atherosclerosis, Cardiovascular disease, heart, pathological conditions

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.