Oxidant stress promotes disease by activating CaMKII
ME Anderson - Journal of molecular and cellular cardiology, 2015 - Elsevier
Journal of molecular and cellular cardiology, 2015•Elsevier
CaMKII is activated by oxidation of methionine residues residing in the regulatory domain.
Oxidized CaMKII (ox-CaMKII) is now thought to participate in cardiovascular and pulmonary
diseases and cancer. This invited review summarizes current evidence for the role of ox-
CaMKII in disease, considers critical knowledge gaps and suggests new areas for inquiry.
Oxidized CaMKII (ox-CaMKII) is now thought to participate in cardiovascular and pulmonary
diseases and cancer. This invited review summarizes current evidence for the role of ox-
CaMKII in disease, considers critical knowledge gaps and suggests new areas for inquiry.
Abstract
CaMKII is activated by oxidation of methionine residues residing in the regulatory domain. Oxidized CaMKII (ox-CaMKII) is now thought to participate in cardiovascular and pulmonary diseases and cancer. This invited review summarizes current evidence for the role of ox-CaMKII in disease, considers critical knowledge gaps and suggests new areas for inquiry.
Elsevier