An Acidic Environment Induces APOL1-Associated Mitochondrial Fragmentation | Zendy

DengFeng Li | Zendy; James A. Snipes | Zendy; Mariana Murea | Zendy; Anthony Molina | Zendy; Jasmin Divers | Zendy; Barry I. Freedman | Zendy; Lijun Ma | Zendy; Snežana Petrović | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

An Acidic Environment Induces <b><i>APOL1</i></b>-Associated Mitochondrial Fragmentation

Author(s) -

DengFeng Li,

James A. Snipes,

Mariana Murea,

Anthony Molina,

Jasmin Divers,

Barry I. Freedman,

Lijun Ma,

Snežana Petrović

Publication year - 2020

Publication title -

american journal of nephrology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.394

H-Index - 85

eISSN - 1421-9670

pISSN - 0250-8095

DOI - 10.1159/000509989

Subject(s) - microbiology and biotechnology , kidney , medicine , biology

Apolipoprotein L1 gene (APOL1) G1 and G2 kidney-risk variants (KRVs) cause CKD in African Americans, inducing mitochondrial dysfunction. Modifying factors are required, because a minority of individuals with APOL1 high-risk genotypes develop nephropathy. Given that APOL1 function is pH-sensitive and the pH of the kidney interstitium is <7, we hypothesized the acidic kidney interstitium may facilitate APOL1 KRV-induced mitochondrial dysfunction.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research