Description

"Mitochondrial ROS-induced Ca2+ influx and microvascular endothelial cell dysfunction in pulmonary arterial hypertension (PAH)" will feature Dr. Karthik Suresh, Assistant Professor of Medicine, Johns Hopkins Medical Institute 

Biography

Dr. Karthik Suresh is a physician-scientist interested in the role of mechanisms of injury and repair in lung microvascular endothelial cells (MVECs) in a variety of diseases. He completed his Internal Medicine residency and Pulmonary/Critical Care fellowship at Johns Hopkins before completing a post-doctoral research fellowship under the guidance of Dr. Larissa Shimoda. Dr. Suresh’s post-doctoral work focused on ROS production and calcium signaling in MVECs, and his current studies explore the mechanistic links between mitochondrial metabolism, elevated ROS and intracellular Ca2+ in MVECs in pre-clinical models of lung injury and pulmonary hypertension. In a separate line of investigation, he also studies mechanisms of lung injury in cancer patients who develop pneumonitis following treatment with immune checkpoint immunotherapy (ICI). Lastly, as an extension of the mitochondrial work in MVECs, his lab also uses computational methods to study mitochondrial genomics in malignant and non-malignant conditions in the lung.

Abstract

Pulmonary arterial hypertension (PAH) is a highly morbid disease characterized by high pulmonary arterial pressures, leading to right ventricular failure and death. Complex, vaso-occlusive lesions in the lung microvasculature are thought to contribute to increased pulmonary vascular pressures in this disease. These lesions are composed of several cell types, including lung microvascular endothelial cells (MVECs). Our lab has focused on mechanisms by which lung MVECs acquire pseudo-oncogenic characteristics (such as increased migration and proliferation) which are thought to drive formation of vaso-occlusive lesions in the lung microvasculature. Specifically, I will discuss our work on how mitochondrial dysfunction and increased intracellular calcium levels may be playing a role in promoting abnormal MVEC function in PAH.