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• W2920609441 startingPage "87" @default.
• W2920609441 abstract "Purpose of review Regression, or reversal, of atherosclerosis has become an important clinical objective. The development of consistent models of murine atherosclerosis regression has accelerated this field of research. The purpose of this review is to highlight recent mouse studies that reveal molecular mechanisms as well as therapeutics targeted for regression. Recent findings Atherosclerosis regression does not involve the same mechanisms as progression in reverse order. Distinct molecular processes within the plaque characterize regression. These processes remained elusive until the advent of murine regression models including aortic transplant, the Reversa mouse, gene complementation and dietary intervention. Studies revealed that depletion of plaque macrophages is a quintessential characteristic of regression, driven by reduced monocyte recruitment into plaques, increased egress of macrophages from plaques and reduced macrophage proliferation. In addition, regression results in polarization of remaining plaque macrophages towards an anti-inflammatory phenotype, smaller necrotic cores and promotion of an organized fibrous cap. Furthermore, type 1 diabetes hinders plaque regression, and several therapeutic interventions show promise in slowing plaque progression or inducing regression. Summary Mouse models of atherosclerosis regression have accelerated our understanding of the molecular mechanisms governing lesion resolution. These insights will be valuable in identifying therapeutic targets aimed at atherosclerosis regression." @default.
• W2920609441 created "2019-03-11" @default.
• W2920609441 creator A5014661710 @default.
• W2920609441 creator A5046009433 @default.
• W2920609441 date "2018-04-01" @default.
• W2920609441 modified "2023-10-01" @default.
• W2920609441 title "Regression of atherosclerosis" @default.
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• W2920609441 doi "https://doi.org/10.1097/mol.0000000000000493" @default.
• W2920609441 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29369832" @default.
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