Schwann cells apoptosis is induced by high glucose in diabetic peripheral neuropathy

Life Sci. 2020 May 1:248:117459. doi: 10.1016/j.lfs.2020.117459. Epub 2020 Feb 21.

Abstract

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes mellitus that affects approximately half of patients with diabetes. Current treatment regimens cannot treat DPN effectively. Schwann cells (SCs) are very sensitive to glucose concentration and insulin, and closely associated with the occurrence and development of type 1 diabetic mellitus (T1DM) and DPN. Apoptosis of SCs is induced by hyperglycemia and is involved in the pathogenesis of DPN. This review considers the pathological processes of SCs apoptosis under high glucose, which include the following: oxidative stress, inflammatory reactions, endoplasmic reticulum stress, autophagy, nitrification and signaling pathways (PI3K/AKT, ERK, PERK/Nrf2, and Wnt/β-catenin). The clarification of mechanisms underlying SCs apoptosis induced by high glucose will help us to understand and identify more effective strategies for the treatment of T1DM DPN.

Keywords: Apoptosis; Diabetic peripheral neuropathy; High glucose; Schwann cells; Signaling pathway.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Autophagy / drug effects
  • Autophagy / genetics
  • Diabetic Neuropathies / complications
  • Diabetic Neuropathies / genetics*
  • Diabetic Neuropathies / metabolism
  • Diabetic Neuropathies / pathology
  • Endoplasmic Reticulum Stress / drug effects
  • Extracellular Signal-Regulated MAP Kinases / genetics
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Gene Expression Regulation
  • Glucose / metabolism
  • Glucose / pharmacology*
  • Humans
  • Hyperglycemia / complications
  • Hyperglycemia / genetics*
  • Hyperglycemia / metabolism
  • Hyperglycemia / pathology
  • Insulin / metabolism
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism
  • Oxidative Stress / drug effects
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Schwann Cells / drug effects*
  • Schwann Cells / metabolism
  • Schwann Cells / pathology
  • Signal Transduction
  • beta Catenin / genetics
  • beta Catenin / metabolism

Substances

  • CTNNB1 protein, human
  • Insulin
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • beta Catenin
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases
  • Glucose