Cellular and molecular mechanisms for rapid regression of atherosclerosis: from bench top to potentially achievable...

Area of Science:

• Cardiovascular Research
• Atherosclerosis Pathophysiology
• Molecular Medicine

Background:

• Decades of research confirm that atherosclerotic lesions, including advanced plaques, can undergo regression and remodeling.
• Recent scientific advancements have elucidated the underlying mechanisms driving plaque regression.

Purpose of the Study:

• To review recent insights into the mechanisms of atherosclerotic plaque regression and remodeling.
• To highlight factors promoting plaque regression and their clinical implications.

Main Methods:

• Review of existing literature on atherosclerotic lesion regression.
• Analysis of molecular and cellular mechanisms involved in plaque regression.
• Synthesis of findings related to lipid metabolism and cellular transport in atherosclerosis.

Main Results:

• Plaque regression is promoted by reduced arterial retention of apolipoprotein B-lipoproteins and enhanced cholesterol efflux.
• Foam cell emigration and subsequent removal of necrotic debris by phagocytes contribute significantly to plaque regression.
• Cellular lipid efflux and foam cell emigration can be rapid following improvements in the plaque environment.

Conclusions:

• Atherosclerotic plaque regression requires significant improvement in the plaque milieu, primarily through reduced atherogenic lipoproteins or enhanced reverse lipid transport.
• Regression processes can rapidly correct features of vulnerable plaques associated with acute coronary syndromes.
• New therapeutic strategies targeting lipoprotein levels and reverse lipid transport could establish plaque regression as a clinical objective.