Swapnil Sonkusare, PhD
Obesity affects about 4 in 10 American adults and 1 in 5 children. Beyond excess weight, it triggers internal changes that can lead to serious health problems. One such change is chronic low-level inflammation, which constricts blood vessels and raises blood pressure. Swapnil Sonkusare, PhD, resident faculty member of the Robert M. Berne Cardiovascular Research Center (CVRC) and professor of molecular physiology and biological physics, recently led a groundbreaking study published in Circulation Research, titled “Paracrine Smooth Muscle-to-Endothelial Signaling via TNF Elevates Blood Pressure in Obesity.” This study identifies a novel inflammatory signaling mechanism that contributes to elevated blood pressure in obesity and highlights the therapeutic potential of targeting this pathway.
Blood vessels are made of concentric layers. Closest to the bloodstream is a layer of endothelial cells, which functions as an internal “skin”, separating flowing blood from the rest of the vessel. These cells become dysfunctional in obesity, contributing to a range of complications. Adjacent to this skin-like layer are smooth muscle cells, which control blood flow and pressure by contracting and relaxing. “When we think about inflammation, we typically focus on immune cells releasing inflammatory signals that affect endothelial or smooth muscle cells,” explains Sonkusare. “We asked a different question: ‘Can endothelial and smooth muscle cells themselves release inflammatory signals that elevate blood pressure?’”
Read the full story on the CVRC website.
Filed Under: Research