Respiratory Critical Care Research Unit
The heart is made up of millions of spontaneously beating cells called cardiomyocytes. They are special cells that share many characteristics with other cell types in our body. For instance, cardiomyocytes contract and relax as calcium concentration goes up and down in the cells, and the energy for contraction and relaxation is derived from mitochondrial respiration.
Cardiomyocytes are known to fail when they are exposed to oxidative stress such as those observed in severe infection (e.g., sepsis) or heart attack, depressing heart function and leading to low blood pressure and poor organ perfusion resistant to treatment. Despite decades of intensive research, the mechanisms responsible for the depressed heart function in sepsis or after heart attack remains poorly understood.
Our research focuses on elucidating molecular mechanisms responsible for the depressed cardiomyocyte function in severe sepsis and other critical illness, including cardiac arrest and cardiopulmonary resuscitation and ischemia and reperfusion injury. Of particular interests are the modulatory roles of nitric oxide (NO) or hydrogen sulfide (H2S)-dependent signals on cellular functions including mitochondrial respiration and calcium handling.
Severe cardiomyocyte dysfunction in acute critical illness is unique because, in most cases, cardiomyocyte function recovers when patients survive. By elucidating the mechanisms responsible for this reversible cardiomyocyte failure, we anticipate finding ways to treat irreversible cellular damage.