APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It?

Article Details

Citation

Copy to clipboard

Olabisi OA, Heneghan JF

APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It?

Semin Nephrol. 2017 Nov;37(6):546-551. doi: 10.1016/j.semnephrol.2017.07.008.

PubMed ID

29110762 [ View in PubMed

]

Abstract

Apolipoprotein L1 (APOL1) protein is the human serum factor that protect human beings against Trypanosoma brucei brucei, the cause of trypanosomiasis. Subspecies of T b brucei that cause human sleeping sickness-T b gambiense and T b rhodesiense evolved molecular mechanisms that enabled them to evade killing by APOL1. Sequence changes (termed G1 and G2) in the APOL1 gene that restored its ability to kill T b rhodesiense also increase the risk of developing glomerular diseases and accelerate progression to end-stage kidney disease. To lyse trypanosome parasites, APOL1 forms pores in the trypanosome endolysosomal and mitochondrial membranes, resulting in rapid membrane depolarization. However, the molecular mechanism underlying APOL1 nephropathy is unknown. Recent experimental evidence has shown that aberrant efflux of intracellular potassium is an early event in APOL1-induced death of human embryonic kidney cells. Here, we discuss the possibility that abnormal efflux of cellular potassium or other cations may be relevant to the pathogenesis of APOL1 nephropathy.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Zinc chloride	Apolipoprotein L1	Protein	Humans	Unknown	Inhibitor	Details
Zinc sulfate, unspecified form	Apolipoprotein L1	Protein	Humans	Unknown	Inhibitor	Details