Review

Impaired RISK-GSK3β Pathway is Responsible for Comorbidities by Suppressing the Conditioning Cardioprotection

Shi-Yun Jin , Ye Zhang
From Department of Anesthesiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, China.
J Anesth Perioper Med 2016; 3(5): 209- 219 . Published on Aug 6, 2016 . doi:10.24015/JAPM.2016.0028
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Abstract

Aim of review: This review elaborates the role of reperfusion injury salvage kinase and glycogen synthase kinase 3β (RISK-GSK3β) pathway in myocardial ischemia/reperfusion injury (IRI) and whether its impairment is responsible for comorbidities due to the suppression of the conditioning cardioprotection.

Method: We review the articles about RISK-GSK3β pathway in myocardial IRI published in the last two decades.

Recent findings: The RISK, including phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and extracellular signal regulated kinase 1/2 (ERK1/2), combines with the downstream target of GSK3β, which confers important role in the conditioning cardioprotection when activated specifically at the time of myocardial reperfusion. Unfortunately, the conditioning protection is weakened or abolished when equipped with comorbidities such as aging, diabetes, obesity, as well as heart diseases. It has been speculated that the pathological processes resulting in RISK-GSK3β pathway alterations may affect the development of IRI and the responses to conditioning.

Summary: The impairment of RISK-GSK3β pathway is responsible for the reduction of conditioning cardioprotection and any strategy that repairs the impairment may have the potential to restore the conditioning against the IRI in the heart in the state of comorbidities.

 

 

Citation: Shi-Yun Jin, and Ye Zhang. Impaired RISK-GSK3β pathway is responsible for comorbidities by suppressing the conditioning cardioprotection. J Anesth Perioper Med 2016; 3: 209-19. doi: 10.24015/JAPM.2016.0028

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