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. Author manuscript; available in PMC: 2021 Jun 21.
Published in final edited form as: Neurosci Lett. 2020 May 26;730:135046. doi: 10.1016/j.neulet.2020.135046

Table 2.

Genes involved in the pathophysiology of brain edema.

Gene Principal role Other diseases related Potential mechanism of edema formation
APOE lipid transport and metabolism [46] cognitive decline, dementia, and Alzheimer’s disease [87, 91], arteriosclerosis, traumatic brain injury, and intracerebral hemorrhage [82, 86, 88] inflammatory response that disrupts the BBB and contributes to vasogenic edema after acute brain injury [92]
Hp acute-phase response and antioxidant role by binding and neutralizing hemoglobin in the blood [72, 93] cardiovascular events [58, 60] oxidative stress [54], the release of inflammatory cytokines, the breakdown of BBB [55]
AQP the main water channel found in the brain, cerebral spinal fluid production and regulation Epilepsy [94], neurological autoimmune diseases[95], diabetes, artherosclerosis[96], cancer [97], peripheral nerves system damage[98] cytotoxic and vasogenic edema, BBB disruption, micro-vessel damage, and neuronal death[65]
Sur1 upregulation after trauma, ischemia, and hypoxia [99] diabetes[99], hypoglycemia[100], autoimmune diseases[101] modulation of astrocyte swelling, a key factor in cytotoxic edema, BBB breakdown and vasogenic edema[73]

APOE – the apolipoprotein gene, Hp- haptoglobin gene, BBB – blood-brain barrier, AQP- aquaporin gene, Sur1- a sulfonylurea receptor and transmembrane protein gene