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Your search for atherosclerosis returned 72 results
Disease: Atherosclerosis susceptibility
Disease Name: Atherosclerosis susceptibility
Pathophysiology comments: Vascular diseases: Atherosclerosis AND aortic aneurysms
Pathophysiology comments: Vascular diseases: Atherosclerosis AND aortic aneurysms
Target:
GPR132 (Class A Orphans)
Consequences of altering gene expression: atherosclerosis in low-density lipoprotein receptor knockout mice. Reduction in aortic lesion coverage, macrophage accumulation
Consequences of altering gene expression: deficiency affects atherosclerosis in a tissue-specific manner. ApoE dependent pro-atherogenic phenotype is observed
Consequences of altering gene expression: ability to engulf apoptotic cells in vitro, and promotes macrophage activation and atherosclerosis in vivo
Consequences of altering gene expression - comment: atherosclerosis. One study investigating GPR132 knockout in LDLR-/- and ApoE-/- mice, suggested an ApoE-dependent
Consequences of altering gene expression: deficiency affects atherosclerosis in a tissue-specific manner. ApoE dependent pro-atherogenic phenotype is observed
Consequences of altering gene expression: ability to engulf apoptotic cells in vitro, and promotes macrophage activation and atherosclerosis in vivo
Consequences of altering gene expression - comment: atherosclerosis. One study investigating GPR132 knockout in LDLR-/- and ApoE-/- mice, suggested an ApoE-dependent
Ligand: darapladib
Comments: clinical drug candidates with potential to reduce the risk of atherosclerosis and associated clinical sequelae .
Clinical use: atherosclerosis, but it failed to meet clinical primary end points and GSK has discontinued further
Immuno Ligand Comments: that may be relevant in conditions other than atherosclerosis that also have an inflammatory component .
Clinical use: atherosclerosis, but it failed to meet clinical primary end points and GSK has discontinued further
Immuno Ligand Comments: that may be relevant in conditions other than atherosclerosis that also have an inflammatory component .
Ligand: inclacumab
Comments: atherosclerosis. It blocks the interaction between selectin P and its primary ligand, P-selectin glycoprotein
Clinical use: atherosclerosis has been terminated. Global Blood Therapeutics redirected development to determine the efficacy of inclacumab
Clinical use: atherosclerosis has been terminated. Global Blood Therapeutics redirected development to determine the efficacy of inclacumab
Target:
regulator of G-protein signaling 1 (R4 family)
Mutations/pathophysiology - disease: Atherosclerosis susceptibility
Mutations/pathophysiology - comment: Vascular diseases: Atherosclerosis AND aortic aneurysms
Mutations/pathophysiology - comment: Vascular diseases: Atherosclerosis AND aortic aneurysms
Target:
regulator of G-protein signaling 5 (R4 family)
Consequences of altering gene expression: Acceleration of disease in atherosclerosis-prone ApoE-/- mice.
Variant: remodeling. Administration of RGS5 shRNA to mice exacerbated a partial carotid ligation model of atherosclerosis
Variant: remodeling. Administration of RGS5 shRNA to mice exacerbated a partial carotid ligation model of atherosclerosis
Target:
P2Y1 receptor (P2Y receptors)
Consequences of altering gene expression: P2Y1 receptor deficiency resulted in a reduction of atherosclerosis in ApoE knockout mice.
Physiological function - description: Atherosclerosis enhancement
Physiological function - description: Atherosclerosis enhancement
Target:
sphingomyelin synthase 2 (Sphingomyelin synthase)
Receptor Immuno Comment: atherosclerosis, fatty liver and insulin resistance. Since downregulation of SMS2 activity results in protective effects
Target:
mixed lineage kinase domain like pseudokinase (TKL-unique family)
Receptor Immuno Comment: atherosclerosis, acute colitis, psoriasis and atherosclerosis . The receptor interacting protein kinases RIPK1 and RIPK3 , and pseudokinase
Ligand: VIP {Sp: Human, Mouse, Rat}
Immuno Ligand Comments: atherosclerosis model, the anti-inflammatory effects of VIP included a reduction in Th1-driven inflammatory
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