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Atherosclerosis: from lesion formation to plaque activation and endothelial dysfunction
1Department of Medicine and Pharmacology, Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, Room W507, Boston, MA 02118, USA.
Insights
Atherosclerosis, a major cause of heart attack and stroke, is still poorly understood. This review examines key theories of atherogenesis and disease activation, focusing on molecular mechanisms for future treatments.
Area of Science:
- Cardiovascular Science
- Molecular Biology
- Pathophysiology
Background:
- Atherosclerosis is a leading cause of morbidity and mortality globally.
- Despite a long-recognized link between LDL cholesterol and atherosclerosis, its precise mechanisms remain unclear.
- Current understanding of atherogenesis is limited, necessitating further investigation into molecular pathways.
Purpose of the Study:
- To review the primary theories of atherogenesis.
- To examine the molecular mechanisms driving atherosclerosis plaque activation.
- To discuss potential therapeutic targets for disease activation amenable to treatment.
Main Methods:
- Review of existing scientific literature on atherogenesis theories.
- Analysis of molecular mechanisms involved in plaque activation and endothelial dysfunction.
- Exploration of murine models for evaluating atherosclerosis hypotheses.
Main Results:
- Identified key working hypotheses of atherosclerosis ready for critical evaluation.
- Highlighted plaque activation and endothelial dysfunction as crucial areas for investigation.
- Emphasized the need for a molecular-level understanding to develop novel interventions.
Conclusions:
- Further research into molecular mechanisms of atherosclerosis is essential.
- Focusing on plaque activation and endothelial dysfunction can lead to next-generation treatments.
- Understanding atherogenesis at a molecular level is key to reducing heart attack and stroke incidence.
Abstract:
Atherosclerosis is an important source of morbidity and mortality in the developed world. Despite the fact that the association between LDL cholesterol and atherosclerosis has been evident for at least three decades, our understanding of exactly how LDL precipitates atherosclerosis is still in its infancy. At least three working hypotheses of atherosclerosis are now nearing the stage where their critical evaluation is possible through a combination of basic science investigation and murine models of atherosclerosis. As we move forward in our understanding of this disease, efforts will be increasingly focused on the molecular mechanisms of disease activation that precipitate the clinical manifestations of atherosclerosis such as heart attack and stroke. Two candidates for such investigation involve the events surrounding plaque activation and endothelial dysfunction. Further investigation in these fields should provide the necessary insight to develop the next generation of interventions that will reduce the clinical manifestations of this devastating disease. The purpose of this work is to review the major theories of atherogenesis, examine the aspects of atherosclerosis that lead to disease activation and discuss aspects of disease activation that are amenable to treatment.