| Symbol
| CD36
| contributors: mct/pgu - updated : 02-04-2016
|
| HGNC name
| CD36 molecule (thrombospondin receptor)
|
| HGNC id
| 1663
|
| corresponding disease(s)
|
CD36D
|
| Other morbid association(s)
|
| Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
|---|
| constitutional
|
|
|
| loss of function
| |
in insulin resistance | | constitutional
|
|
| --low
|
| |
in PWS point to an abnormal control of lipid and glucose homeostasis which may explain the insatiable hunger in these patients | | constitutional
|
|
| --low
|
|
reduced the capability of monocytes to phagocyte apoptotic neutrophils  | |
| Susceptibility
|
to severe malaria, cerebral form to atherosclerosis to insulin resistance to hypertension |
| Variant & Polymorphism
SNP
| 14T/C and 53G/T increase the risk of cerebral malaria |
|
AGGIG haplotype modulating lipid metabolism and cardiovascular risk |
|
mutations within the kidney can increase blood pressure |
|
SNPs of CD36 are associated with metabolic syndrome in Puerto Ricans |
| 
|
| Candidate gene
| high soluble CD36 is associated with increased type 2 diabetes risk |
|
involved in sterile inflammation through assembly of TLR4/TLR6 heterodimer in atherosclerosis and Alzeihmer's disease |
Marker
Therapy target
|
|
| System | Type | Disorder | Pubmed |
|---|
| cardiovascular | aquired | | |
| target for treatment and/or prevention of cardiovascular disease | | diabete | type 2 | | |
| novel therapeutic strategies aimed at reducing CD36-mediated fatty acids uptake show promise for the prevention or treatment of cardiac dysfunction related to obesity and diabetes | | diabete | type 2 | | |
| novel and potential therapeutic target for diabetic renal tubule fibrosis | | neurology | neurodegenerative | alzheimer | |
| potential therapeutical target to counteract the cerebrovascular dysfunction associated with APP. | | neurology | neurodegenerative | | |
| is a putative therapeutic target for cerebral amyloid angiopathy (CAA) |
| | |
|
| CD36 is necessary for the development of lipotoxic cardiomyopathy in MHC-PPARalpha mice | |
Cd36 deletion ameliorates cerebrovascular function in Tg2576 mice at an age marked by extensive amyloid deposition in brain and cerebral blood vessels |