Abstract
Pyroptosis is a novel programmed cell death process that promotes the release of interleukin-1β (IL-1β) and interleukin-18 (IL-18) by activating inflammasomes and gasdermin D (GSDMD), leading to cell swelling and rupture. Pyroptosis is involved in the regulation of the occurrence and development of cardiovascular and cerebrovascular diseases, tumors, and nerve injury. Diabetes is a metabolic disorder characterized by long-term hyperglycemia, insulin resistance, and chronic inflammation. The people have paid more and more attention to the relationship between pyroptosis, diabetes, and its complications, especially its important regulatory significance in diabetic neurological diseases, such as diabetic encephalopathy (DE) and diabetic peripheral neuropathy (DPN). This article will give an in-depth overview of the relationship between pyroptosis, diabetes, and its related neuropathy, and discuss the regulatory pathway and significance of pyroptosis in diabetes-associated neuropathy.
Highlights
Diabetes is a metabolic disorder characterized by hyperglycemia and insulin resistance
We found that mitochondrial damage-induced excessive reactive oxygen species (ROS) level is an important induction mechanism of diabetes-induced nerve damage, such as diabetes-associated cognitive dysfunction
Our study found that fibroblast growth factor 1 (FGF1) expression is significantly inhibited after diabetic peripheral neuropathy (DPN), and exogenous FGF1 could alleviate DPN by alleviating oxidative stress in Schwann cells (SCs) (Li et al, 2021)
Summary
Diabetes is a metabolic disorder characterized by hyperglycemia and insulin resistance. The overexpression of TXNIP induces the activation of NLRP3 inflammasome in the injured spinal cord and triggers the neuronal cell death dependent on pyroptosis (Yanagisawa et al, 2019). High glucose stimulation can activate NLRP3 inflammasome, trigger the pyroptosis of retinal microglial cell and lead to diabetic retinopathy (DR) (Huang et al, 2021).
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