ReviewARYA atherosclerosis2022
A Systematic Review of Apolipoprotein A-I Mimetic Peptides for Atherosclerosis Therapy via Activation of the Reverse Cholesterol Transport Pathway.
Review in ARYA atherosclerosis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHDL has been identified a s a p otential n ew t reatment f or atherosclerosis. Targeting lipid metabolism via the Reverse Cholesterol Transport (RCT) pathway can improve HDL metabolism. Apolipoprotein A-I mimetic peptides (ApoA-I MPs) are able to increase HDL metabolism. Thus, this systematic review aimed to examine the potential effect o f A poA-I M Ps a gainst a therosclerosis i n mice models through the RCT mechanism.
methodThis systematic review was conducted using previous in vivo studies published in four scientific databases over the last ten years (PubMed, SCOPUS, ProQuest, and Science Direct) and was based on the Systematic Review Protocol for Animal Intervention Studies (SYRCLE) protocol.
resultsThis study's primary outcome was a reduction in atherosclerotic plaque, where 16 articles were qualified for this study. Based on the risk of bias analysis, these articles had a low risk of bias. Most in vivo studies (13 of 16) showed that ApoA-I MPs significantly reduced atherosclerotic plaque formation. Generally, ApoA-I MPs played an important role in regulating HDL metabolism (HDL remodeling process, increased cholesterol efflux, and stimulated RC T pathway) and an ti-inflammatory agent. Apo A-I MPs may differ in their ability to reduce atherosclerotic plaque depending on the peptide sequence and administration route.
conclusionsApoA-I MPs can reduce atherosclerotic plaque formation in mice by increasing cholesterol efflux vi a th e RC T pa thway. Fu rther in vestigation is re quired to su pport th e de velopment of ApoA-I MPs as a new therapy for atherosclerosis in humans.
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