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Article: Targeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products

TitleTargeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products
Authors
Keywordsanimal model
arteriosclerosis
atherosclerosis
cholesterol transport
cholesterol esterification
Issue Date2019
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://www.pharmrev.org/
Citation
Pharmacological Reviews, 2019, v. 71 n. 4, p. 596-670 How to Cite?
AbstractFoam cell formation and further accumulation in the subendothelial space of the vascular wall is a hallmark of atherosclerotic lesions. Targeting foam cell formation in the atherosclerotic lesions can be a promising approach to treat and prevent atherosclerosis. The formation of foam cells is determined by the balanced effects of three major interrelated biologic processes, including lipid uptake, cholesterol esterification, and cholesterol efflux. Natural products are a promising source for new lead structures. Multiple natural products and pharmaceutical agents can inhibit foam cell formation and thus exhibit antiatherosclerotic capacity by suppressing lipid uptake, cholesterol esterification, and/or promoting cholesterol ester hydrolysis and cholesterol efflux. This review summarizes recent findings on these three biologic processes and natural products with demonstrated potential to target such processes. Discussed also are potential future directions for studying the mechanisms of foam cell formation and the development of foam cell-targeted therapeutic strategies.
Persistent Identifierhttp://hdl.handle.net/10722/277731
ISSN
2021 Impact Factor: 18.923
2020 SCImago Journal Rankings: 8.176
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWang, D-
dc.contributor.authorYang, Y-
dc.contributor.authorLei, Y-
dc.contributor.authorTzvetkov, NT-
dc.contributor.authorLiu, X-
dc.contributor.authorYeung, AWK-
dc.contributor.authorXu, S-
dc.contributor.authorAtanasov, AG-
dc.date.accessioned2019-10-04T08:00:11Z-
dc.date.available2019-10-04T08:00:11Z-
dc.date.issued2019-
dc.identifier.citationPharmacological Reviews, 2019, v. 71 n. 4, p. 596-670-
dc.identifier.issn0031-6997-
dc.identifier.urihttp://hdl.handle.net/10722/277731-
dc.description.abstractFoam cell formation and further accumulation in the subendothelial space of the vascular wall is a hallmark of atherosclerotic lesions. Targeting foam cell formation in the atherosclerotic lesions can be a promising approach to treat and prevent atherosclerosis. The formation of foam cells is determined by the balanced effects of three major interrelated biologic processes, including lipid uptake, cholesterol esterification, and cholesterol efflux. Natural products are a promising source for new lead structures. Multiple natural products and pharmaceutical agents can inhibit foam cell formation and thus exhibit antiatherosclerotic capacity by suppressing lipid uptake, cholesterol esterification, and/or promoting cholesterol ester hydrolysis and cholesterol efflux. This review summarizes recent findings on these three biologic processes and natural products with demonstrated potential to target such processes. Discussed also are potential future directions for studying the mechanisms of foam cell formation and the development of foam cell-targeted therapeutic strategies.-
dc.languageeng-
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://www.pharmrev.org/-
dc.relation.ispartofPharmacological Reviews-
dc.subjectanimal model-
dc.subjectarteriosclerosis-
dc.subjectatherosclerosis-
dc.subjectcholesterol transport-
dc.subjectcholesterol esterification-
dc.titleTargeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products-
dc.typeArticle-
dc.identifier.emailYeung, AWK: ndyeung@hku.hk-
dc.identifier.authorityYeung, AWK=rp02143-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1124/pr.118.017178-
dc.identifier.pmid31554644-
dc.identifier.scopuseid_2-s2.0-85072662034-
dc.identifier.hkuros306843-
dc.identifier.volume71-
dc.identifier.issue4-
dc.identifier.spage596-
dc.identifier.epage670-
dc.identifier.isiWOS:000500540700007-
dc.publisher.placeUnited States-
dc.identifier.issnl0031-6997-

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