Apoptosis induced by endoplasmic reticulum stress involved in diabetic kidney disease

Guanghui Liu1, Yingying Sun, Zhenhua Li

  • 1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University, Qilu Hospital, Wenhua Xi Road, Jinan, Shandong 250012, PR China.

Insights

Endoplasmic reticulum stress contributes to kidney damage in diabetic nephropathy. This study found increased ER stress and apoptosis in the kidneys of diabetic rats, suggesting a role in disease development.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Endocrinology

Background:

  • Diabetic complications are linked to endoplasmic reticulum (ER) stress.
  • The role of ER stress in diabetic nephropathy-induced kidney injury remains unclear.

Purpose of the Study:

  • To investigate the involvement of ER-associated apoptosis in streptozotocin-induced diabetic nephropathy in rats.
  • To analyze key markers of ER stress and apoptosis in the kidneys of diabetic rats.

Main Methods:

  • Streptozotocin-induced diabetic rat model.
  • Assessment of albuminuria, kidney histology (H&E), and apoptosis (TUNEL assay).
  • Immunohistochemistry, Western blot, and real-time PCR for ER stress markers (GRP78, CHOP, JNK, caspase-12).

Main Results:

  • Diabetic rats exhibited signs of nephropathy and increased kidney apoptosis.
  • Significant upregulation of the ER chaperone GRP78 was observed in diabetic kidneys.
  • Key ER-associated apoptosis markers (CHOP, JNK, caspase-12) were activated in diabetic kidneys.

Conclusions:

  • Apoptosis induced by ER stress occurs in the kidneys of diabetic rats.
  • ER stress-mediated apoptosis may play a significant role in the pathogenesis of diabetic nephropathy.

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