 Apolipoprotein A-I
"Apolipoprotein A-I" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.
| Descriptor ID |
D016632
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| MeSH Number(s) |
D10.532.091.200.100 D12.776.070.400.200.100 D12.776.521.120.200.100
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| Concept/Terms |
Apolipoprotein A-I- Apolipoprotein A-I
- Apolipoprotein A I
- Apo A-I
- Apo A1
- Apolipoprotein AI
- ApoA-1
- ApoA-I
- Apolipoprotein A-1
- Apolipoprotein A 1
- Apolipoprotein A1
- Apo A-1
- Apo AI
Pro-Apolipoprotein A-I- Pro-Apolipoprotein A-I
- Pro Apolipoprotein A I
- Pro-Apo A-I
- Pro Apo A I
- Proapolipoprotein AI
- Apolipoprotein AI Propeptide
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Below are MeSH descriptors whose meaning is more general than "Apolipoprotein A-I".
Below are MeSH descriptors whose meaning is more specific than "Apolipoprotein A-I".
This graph shows the total number of publications written about "Apolipoprotein A-I" by people in this website by year, and whether "Apolipoprotein A-I" was a major or minor topic of these publications.
To see the data from this visualization as text, click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 2014 | 1 | 1 | 2 | | 2015 | 1 | 0 | 1 | | 2016 | 0 | 1 | 1 | | 2019 | 0 | 1 | 1 | | 2021 | 1 | 0 | 1 |
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Below are the most recent publications written about "Apolipoprotein A-I" by people in Profiles.
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Li L, Cai G, Lu W, Li F, Yu L, Xiao J. The ratio of HDL-C to apoA-I interacts with free triiodothyronine to modulate coronary artery disease risk. BMC Cardiovasc Disord. 2021 10 19; 21(1):504.
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Sposito AC, Carmo HR, Barreto J, Sun L, Carvalho LSF, Feinstein SB, Zanotti I, Kontush A, Remaley A. HDL-Targeted Therapies During Myocardial Infarction. Cardiovasc Drugs Ther. 2019 06; 33(3):371-381.
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O'Donnell MJ, Chin SL, Rangarajan S, Xavier D, Liu L, Zhang H, Rao-Melacini P, Zhang X, Pais P, Agapay S, Lopez-Jaramillo P, Damasceno A, Langhorne P, McQueen MJ, Rosengren A, Dehghan M, Hankey GJ, Dans AL, Elsayed A, Avezum A, Mondo C, Diener HC, Ryglewicz D, Czlonkowska A, Pogosova N, Weimar C, Iqbal R, Diaz R, Yusoff K, Yusufali A, Oguz A, Wang X, Penaherrera E, Lanas F, Ogah OS, Ogunniyi A, Iversen HK, Malaga G, Rumboldt Z, Oveisgharan S, Al Hussain F, Magazi D, Nilanont Y, Ferguson J, Pare G, Yusuf S. Global and regional effects of potentially modifiable risk factors associated with acute stroke in 32 countries (INTERSTROKE): a case-control study. Lancet. 2016 Aug 20; 388(10046):761-75.
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Castle JW, Kent KP, Fan Y, Wallace KD, Davis CE, Roberts JC, Marino ME, Thomenius KE, Lim HW, Coles E, Davidson MH, Feinstein SB, DeMaria A. Therapeutic ultrasound: Increased HDL-Cholesterol following infusions of acoustic microspheres and apolipoprotein A-I plasmids. Atherosclerosis. 2015 Jul; 241(1):92-9.
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Reiser J, Nast CC, Alachkar N. Permeability factors in focal and segmental glomerulosclerosis. Adv Chronic Kidney Dis. 2014 Sep; 21(5):417-21.
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Castle J, Feinstein SB. Ultrasound-directed, site-specific gene delivery. Methods Mol Biol. 2014; 1141:67-76.
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