Open AccessInvolvement of Notch1 and ALK4/5 Signaling Pathways in Renal Tubular Cell Death: Their Application to Clarification of Cadmium Toxicity
Author(s) -
Kazuo Fujiki
Publication year - 2020
Publication title -
nippon eiseigaku zasshi/nihon eiseigaku zasshi
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.168
H-Index - 17
eISSN - 1882-6482
pISSN - 0021-5082
DOI - 10.1265/jjh.20007
Subject(s) - cadmium , toxicity , cadmium poisoning , microbiology and biotechnology , signal transduction , cancer research , cell , chemistry , pharmacology , toxicology , medicine , biology , biochemistry , organic chemistry
Renal tubular cell death is caused by various extracellular stresses including toxic amounts of cadmium, an occupational and environmental pollutant metal, and is responsible for renal dysfunction. While cadmium exposure disrupts many intracellular signaling pathways, the molecular mechanism underlying cadmium-induced renal tubular cell death has not yet been fully elucidated. We have recently identified two important intracellular signaling pathways that promote cadmium-induced renal tubular cell death: the Notch1 signaling and activin receptor-like kinase (ALK) 4/5 signaling (also known as the activin-transforming growth factor β receptor pathways). In this review paper, we introduce our previous experimental findings, focusing on Notch1 and ALK4/5 signaling pathways, which may uncover the molecular mechanisms involved in cadmium-induced renal tubular cell death.