Surface-modified particles loaded with CaMKII inhibitor protect cardiac cells against mitochondrial injury.

ABSTRACT: An excess of calcium (Ca²⁺) influx into mitochondria during mitochondrial re-energization is one of the causes of myocardial cell death during ischemic/reperfusion injury. This overload of Ca²⁺ triggers the mitochondrial permeability transition pore (mPTP) opening which leads to programmed cell death. During the ischemic/reperfusion stage, the activated Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) enzyme is responsible for Ca²⁺ influx. To reduce CaMKII-related cell death, sub-micron particles composed of poly(lactic-co-glycolic acid) (PLGA), loaded with a CaMKII inhibitor peptide were fabricated. The CaMKII inhibitor peptide-loaded (CIP) particles were coated with a mitochondria targeting moiety, triphenylphosphonium cation (TPP), which a

SUBMITTER: Wongrakpanich A 

PROVIDER: S-EPMC5401631 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature