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Human apolipoprotein L1 (ApoL1) in cancer and chronic kidney disease
Author(s) -
Hu Chien-An A.,
Klopfer Edward I.,
Ray Patricio E.
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.03.002
Subject(s) - autophagy , kidney disease , biology , homeostasis , disease , kidney , cancer , cancer research , immunology , bioinformatics , medicine , genetics , microbiology and biotechnology , endocrinology , pathology , apoptosis
Human apolipoprotein L1 (ApoL1) possesses both extra‐ and intra‐cellular functions crucial in host defense and cellular homeostatic mechanisms. Alterations in ApoL1 function due to genetic, environmental, and lifestyle factors have been associated with African sleeping sickness, atherosclerosis, lipid disorders, obesity, schizophrenia, cancer, and chronic kidney disease (CKD). Importantly, two alleles of APOL1 carrying three coding‐sequence variants have been linked to CKD, particularly in Sub‐Saharan Africans and African Americans. Intracellularly, elevated ApoL1 can induce autophagy and autophagy‐associated cell death, which may be critical in the maintenance of cellular homeostasis in the kidney. Similarly, ApoL1 may protect kidney cells against renal cell carcinoma (RCC). We summarize the role of ApoL1 in RCC and CKD, highlighting the critical function of ApoL1 in autophagy.