Mitochondrial proteins that connected with calcium: do their pathways changes in PAH?

University of Glasgow, G12 8QQ, UK

Abstract

Calcium can be regulated by mitochondria and also plays a significant role in mitochondrial pathways. Recent study showed mitochondrial protein changes in the right ventricle in pulmonary arterial hypertension, which affects calcium network at the same time. The specific objective of this study is to assess the pathway of calcium transport by permeable pore in mitochondria and investigate the regulation of mitochondrial proteins in order to find the connection between mitochondrial proteins and right ventricular dysfunction in PAH (pulmonary arterial hypertension). This literature-based review came out by searching articles in Pubmed and Science Direct. And the related flow chart is expressed by the form of PRISMA. There is a network between mitochondria and calcium through the transport chain called mitochondria permeability transition pore (MPTP) as well as different kinds of proteins that are located in the mitochondria. MPTP is a kind of mitochondria pore and can have conformational changes after protein phosphorylation or reaction between mitochondrial proteins to activate the apoptosis capase cascade process in cell death. In addition, MPTP can be activated by other mitochondrial protein like signal transducer activator of transcription3 (STAT3) to activate cytochrome c in pro-apoptosis to initiate cell death at the same time. The most obvious finding from this study is the role of calcium regulation in therapeutic treatment in PAH patients, which suggest an imaginable role for calcium transporter like mitochondria calcium uniporter (MCU) promoting bio-markers in cardiovascular disease resulting from mitochondrial dysfunction. In addition, right ventricle is a target of PAH in which mitochondria in RV would play an essential role in pathways such as ATP production via mitochondria metabolism.