Autophagy Induced by ROS Aggravates Testis Oxidative Damage in Diabetes via Breaking the Feedforward Loop Linking p62

Yuanyuan Tian1, Wei Song1, Dongsheng Xu1

  • 1Cancer Center, The First Hospital of Jilin University, Changchun, Jilin 130021, China.

Insights

Diabetic male infertility stems from testicular dysfunction. This review explores how oxidative stress and autophagy disrupt testicular function via the PI3K/Akt/mTOR pathway, leading to damage.

Area of Science:

  • Reproductive Biology
  • Endocrinology
  • Cellular Biology

Background:

  • Hyperglycemia-induced testicular dysfunction is a primary cause of infertility in diabetic men.
  • Existing treatments for diabetic male infertility lack comprehensive safety, efficacy, and practicality.
  • Understanding the underlying mechanisms is crucial for developing effective interventions.

Purpose of the Study:

  • To elucidate the mechanisms of male infertility in diabetes.
  • To investigate the roles of oxidative stress and autophagy in diabetic testicular dysfunction.
  • To analyze the involvement of the PI3K/Akt/mTOR signaling pathway.

Main Methods:

  • Review of current scientific literature on diabetic male infertility.
  • Focus on cellular and molecular pathways involved in testicular function.
  • Analysis of the interplay between oxidative stress, autophagy, and signaling pathways.

Main Results:

  • Diabetes-induced hyperglycemia leads to oxidative stress in the testes.
  • Oxidative stress triggers dysregulated autophagy, impacting testicular function.
  • The PI3K/Akt/mTOR signaling pathway is implicated in mediating these effects.
  • Autophagy disruption breaks the Nrf2 and p62 feedback loop, exacerbating oxidative damage.

Conclusions:

  • Diabetic male infertility involves complex interactions between oxidative stress and autophagy.
  • The PI3K/Akt/mTOR pathway is a key regulator in this process.
  • Targeting oxidative stress and autophagy may offer novel therapeutic strategies for diabetic male infertility.