How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia

Metab Brain Dis. 2021 Oct;36(7):1445-1467. doi: 10.1007/s11011-021-00770-z. Epub 2021 Jun 26.

Abstract

Ischemic stroke is the second leading cause of mortality and disability globally. Neuronal damage following ischemic stroke is rapid and irreversible, and eventually results in neuronal death. In addition to activation of cell death signaling, neuroinflammation is also considered as another pathogenesis that can occur within hours after cerebral ischemia. Under physiological conditions, subcellular organelles play a substantial role in neuronal functionality and viability. However, their functions can be remarkably perturbed under neurological disorders, particularly cerebral ischemia. Therefore, their biochemical and structural response has a determining role in the sequel of neuronal cells and the progression of disease. However, their effects on cell death and neuroinflammation, as major underlying mechanisms of ischemic stroke, are still not understood. This review aims to provide a comprehensive overview of the contribution of each organelle on these pathological processes after ischemic stroke.

Keywords: Cell death; Cellular organelles; Cerebral ischemia; Neuroinflammation; Stroke.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Death
  • Cytosol / physiology
  • Endoplasmic Reticulum / physiology
  • Golgi Apparatus / physiology
  • Humans
  • Ischemic Stroke / complications
  • Ischemic Stroke / etiology
  • Ischemic Stroke / pathology*
  • NLR Family, Pyrin Domain-Containing 3 Protein / physiology
  • Neuroinflammatory Diseases / etiology
  • Neuroinflammatory Diseases / prevention & control*
  • Neurons / pathology*
  • Organelles / physiology*
  • Peroxisomes / physiology
  • Ribosomes / physiology

Substances

  • NLR Family, Pyrin Domain-Containing 3 Protein