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Mechanistic Implications of GSK and CREB Crosstalk in Ischemia Injury

Heena Khan1, Annu Bangar1, Amarjot Kaur Grewal1

  • 1Chitkara College of Pharmacy, Chitkara University, Punjab, 140401, India.

Neurotoxicity Research
|December 13, 2023
PubMed

Insights

Ischemia-reperfusion injury causes cell death, but activating the GSK/CREB pathway enhances cell survival. This pathway offers a promising strategy for managing organ damage after reduced blood flow.

Area of Science:

  • Cellular Biology
  • Physiology
  • Pathology

Background:

  • Ischemia-reperfusion (IR) injury results from insufficient blood supply, causing cellular dysfunction and death in organs like the kidney, liver, and brain.
  • IR injury triggers cellular stress, including oxidative stress, calcium overload, inflammation, and apoptosis, potentially leading to systemic damage.
  • Dysfunction of cyclic AMP response element (CRE)-binding protein (CREB) signaling is implicated in various diseases, including IR injury.

Purpose of the Study:

  • To explore the protective role of the GSK/CREB signaling pathway in mitigating ischemia-reperfusion injury.
  • To investigate the involvement of GSK-3 and CREB in various signaling pathways altered during IR injury.
  • To highlight the crosstalk between GSK-3 and CREB in promoting cell survival and resistance to ischemia.

Main Methods:

  • Review of existing literature on signaling pathways involved in IR injury.
  • Analysis of the modulation of GSK-3 and CREB in response to IR.
  • Examination of the role of calcium-calmodulin-dependent protein kinase (CaMK) in CREB activation.

Main Results:

  • Activation of CREB promotes cell survival and enhances resistance to ischemic conditions.
  • GSK-3 and CREB act as downstream targets in multiple signaling pathways affected by IR injury.
  • Calcium overload during ischemia activates CaMK, which in turn activates CREB-mediated transcription, promoting cell survival.

Conclusions:

  • The GSK/CREB signaling pathway demonstrates significant protective potential for cells in various organs following ischemia.
  • Targeting the GSK/CREB pathway represents a futuristic strategy for managing ischemia-reperfusion injury.
  • The crosstalk between GSK-3 and CREB is crucial for enhancing cell survival and conferring resistance to subsequent ischemic events.

Keywords:
CREBDephosphorylationGSK-3βIschemia-reperfusion injuryPhosphorylation

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