Open AccessManifestation of renin angiotensin system modulation in traumatic brain injury
Author(s) -
Golnoush Mirzahosseini,
Saifudeen Ismael,
Heba A. Ahmed,
Tauheed Ishrat
Publication year - 2021
Publication title -
metabolic brain disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.851
H-Index - 67
eISSN - 1573-7365
pISSN - 0885-7490
DOI - 10.1007/s11011-021-00728-1
Subject(s) - neuroinflammation , angiotensin ii , proinflammatory cytokine , traumatic brain injury , angiotensin ii receptor type 1 , medicine , neuroscience , oxidative stress , angiotensin receptor , renin–angiotensin system , receptor , inflammation , endocrinology , biology , psychiatry , blood pressure
Traumatic brain injury (TBI) alters brain function and is a crucial public health concern worldwide. TBI triggers the release of inflammatory mediators (cytokines) that aggravate cerebral damage, thereby affecting clinical prognosis. The renin angiotensin system (RAS) plays a critical role in TBI pathophysiology. RAS is widely expressed in many organs including the brain. Modulation of the RAS in the brain via angiotensin type 1 (AT 1 ) and type 2 (AT 2 ) receptor signaling affects many pathophysiological processes, including TBI. AT 1 R is highly expressed in neurons and astrocytes. The upregulation of AT 1 R mediates the effects of angiotensin II (ANG II) including release of proinflammatory cytokines, cell death, oxidative stress, and vasoconstriction. The AT 2 R, mainly expressed in the fetal brain during development, is also related to cognitive function. Activation of this receptor pathway decreases neuroinflammation and oxidative stress and improves overall cell survival. Numerous studies have illustrated the therapeutic potential of inhibiting AT 1 R and activating AT 2 R for treatment of TBI with variable outcomes. In this review, we summarize studies that describe the role of brain RAS signaling, through AT 1 R and AT 2 R in TBI, and its modulation with pharmacological approaches.