Inflammation-induced PINCH expression leads to actin depolymerization and mitochondrial mislocalization in neurons.
Kalimuthusamy NatarajaseenivasanSanthanam ShanmughapriyaPrema VelusamyMatthew SayreAlvaro GarciaNestor Mas GomezT Dianne LangfordPublished in: Translational neurodegeneration (2020)
This study reported for the first time the mechanistic and biological consequences of PINCH expression in CNS neurons in diseases with a chronic neuroinflammation component. Our findings point to the maintenance of PINCH at normal physiological levels as a potential new therapeutic target for neurodegenerative diseases with impaired metabolisms.
Keyphrases
- poor prognosis
- oxidative stress
- spinal cord
- diabetic rats
- binding protein
- traumatic brain injury
- drug induced
- long non coding rna
- high glucose
- lipopolysaccharide induced
- blood brain barrier
- lps induced
- spinal cord injury
- cognitive impairment
- endothelial cells
- climate change
- cerebral ischemia
- inflammatory response
- cell migration
- human health
- subarachnoid hemorrhage