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Hypertension is called the "silent killer"; it is the most common complication of cardiovascular diseases such as stroke and heart failure. Over 30% of the population in the Western world suffers from hypertension; unfortunately, the etiology of most cases remains uncertain. It is well appreciated that the central nervous system is essential in regulating blood pressure; renal sympathetic denervation has produced significant blood pressure lowering in treatment-resistant hypertensive patients. However, the cause of the disruption of the central regulation of blood pressure in hypertension is unclear. The Shi Laboratory is exploring the brain mechanism by targeting microglia—the innate resident immune cells—during the development of hypertension. Our previous work indicates that anti-inflammation in the central nervous system could significantly suppress blood pressure and sympathetic tone in the hypertensive animals.
To gain deeper understanding of the involvement of microglia, neuroinflammation and associated molecular events in the progress of hypertension, our research goals are to:
- Examine the effects of microglia on sympathetic outflow, neurohumoral release and pathophysiological changes associated with hypertension
- Characterize a distinctive molecular signature of microglial activation associated with hypertension
- Understand how microglial activation changes the progress of hypertension and its molecular basis
Diphtheria Toxin (DT)-induced microglial apoptosis in the hypothalamic PVN
Iba1: A microglial marker