Microglia are the resident immune cells within the brain and retina, commonly known as the macrophages of the central nervous system (CNS).1 Microglia survey the surrounding milieu to eliminate invading microbes, clear cellular debris and enforce programmed cell death by removing apoptotic cells.1, 2 Complementary to their house-keeping role, microglia are capable of releasing brain derived neurotrophic factor (BDNF), as well as various anti-inflammatory cytokines which sustain and support neuronal survival.3-5 While they are essential for maintaining a healthy CNS, paradoxically they may undergo phenotypic changes to influence numerous neurodegenerative disorders, including Parkinson s6 and Alzheimer s7 disease. Understanding the underlying mechanisms that determine whether microglia are supportive or toxic could elucidate novel and more effective therapeutic targets to treat an array of neurological and retinal diseases. Although relatively little is known about the influences that evoke phenotypical changes in the microglial population, there is an accumulating amount of evidence illustrating an interaction with the Renin-Angiotensin system (RAS).8 The angiotensin type 1 receptor (AT1R) and angiotensin type 2 receptor (AT2R) may have differential roles in mediating the activity of microglia. Understanding the actions of these angiotensin receptors will be important in defining whether microglia are an important therapeutic for RAS blockade in brain and ocular diseases.
|Pages (from-to)||571 - 579|
|Number of pages||9|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 2013|