ApoL1 and the Immune Response of Patients with Systemic Lupus Erythematosus.
Curr Rheumatol Rep
; 19(3): 13, 2017 Mar.
Article
in En
| MEDLINE
| ID: mdl-28265848
ABSTRACT
PURPOSE OF REVIEW Systemic lupus erythematosus (SLE) confers up to a 50-fold increased risk of cardiovascular disease (CVD), and African Americans with SLE experience accelerated damage accrual and doubled cardiovascular risk when compared to their European American counterparts. RECENT FINDINGS:
Genome-wide association studies have identified a substantial signal at 22q13, now assigned to variation at apolipoprotein L1 (APOL1), which has associated with progressive nondiabetic nephropathy, cardiovascular disease, and many immune-associated renal diseases, including lupus nephritis. We contend that alterations in crucial APOL1 intracellular pathways may underpin associated disease states based on structure-functional differences between variant and ancestral forms. While ancestral APOL1 may be a key driver of autophagy, nonconserved primary structure changes result in a toxic gain of function with attenuation of autophagy and an unsupervised pore-forming feature. Thus, the divergent intracellular biological pathways of ancestral and variant APOL1 may explain a worsened prognosis as demonstrated in SLE.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Apolipoproteins
/
Lipoproteins, HDL
/
Lupus Erythematosus, Systemic
Type of study:
Prognostic_studies
Limits:
Humans
Language:
En
Journal:
Curr Rheumatol Rep
Journal subject:
REUMATOLOGIA
Year:
2017
Document type:
Article
Affiliation country: