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HMGB1 plays an important role in pyroptosis induced blood brain barrier breakdown in diabetes-associated cognitive decline.
- Source :
-
Journal of Neuroimmunology . Jan2022, Vol. 362, pN.PAG-N.PAG. 1p. - Publication Year :
- 2022
-
Abstract
- Diabetes mellitus increases the risk of dementia, and evidence suggests hyperglycemia is a key contributor to neurodegeneration. However, our understanding of diabetes-associated cognitive decline, an important complication of diabetes mellitus, is lacking and the underlying mechanism is unclear. Blood brain barrier (BBB) breakdown is a possible cause of dementia in diabetes mellitus and Alzheimer's disease. Accumulating evidence shows BBB dysfunction caused by hyperglycemia contributes to cognitive decline. A specific type of inflammatory programmed cell death, called pyroptosis, has potential as a therapeutic target for BBB-associated diseases. Potential inducers of pyroptosis include inflammasomes such as NLRP3, whose activation relies on damage-associated molecular patterns. High mobility group box 1 (HMGB1) is a highly conserved, ubiquitous protein found in most cell types, and acts as a damage-associated molecular pattern when released from the nucleus. We propose that HMGB1 influences vascular inflammation by activating the NLRP3 inflammasome and thereby initiating pyroptosis in vascular cells. Moreover, HMGB1 plays a pivotal role in the pathogenesis of diabetes mellitus and diabetic complications. Here, we review the role of HMGB1 in BBB dysfunction induced by hyperglycemia and propose that HMGB1 is a promising therapeutic target for countering diabetes-associated cognitive decline. [Display omitted] • Diabetes mellitus makes a contribution to blood brain barrier breakdown. • Blood brain barrier disturbances in diabetes could be the possible link between dementia and diabetes. • Pyroptosis contributes to hyperglycemia induced BBB breakdown. • HMGB1 plays an important role in pyroptosis of injured blood brain barrier via activating NLRP3 inflammasome. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 01655728
- Volume :
- 362
- Database :
- Academic Search Index
- Journal :
- Journal of Neuroimmunology
- Publication Type :
- Academic Journal
- Accession number :
- 154338653
- Full Text :
- https://doi.org/10.1016/j.jneuroim.2021.577763