Of the nearly one million people in the United States who are affected by sepsis each year, almost one-fifth die. Cardiovascular complications account for approximately 80 percent of those deaths. The heart muscle, weakened by systemic inflammation, is unable to generate the energy it needs to contract, resulting in a severe decline in blood flow and oxygen delivery to tissues that ultimately leads to organ failure. Now, in new work, scientists at the Lewis Katz School of Medicine at Temple University (LKSOM), in collaboration with colleagues at Columbia University in New York, describe the mechanism underlying the loss of energy from heart dysfunction in sepsis, opening the way for the development of a new therapy that could save thousands of lives annually.
“Currently, the main approach to the treatment of sepsis is supportive,” Dr. Drosatos said. “With our latest findings, supportive and anti-inflammatory treatments would remain a mainstay, but by also ensuring that the heart is producing energy, we could provide extra time for the treatments to work before the heart fails.”
Dr. Drosatos and colleagues are now turning their attention to humans, expanding their research in human cells. “If the treatments are beneficial, as they have been in mice, we hope to soon be interacting with clinical groups to translate our studies to human patients,” he said.