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KLF11 protects chondrocytes via inhibiting p38 MAPK signaling pathway

F Han1, H Jiang, W Qu

  • 1Soochow University, Suzhou, China. Yongjunsoochow@163.com.

European Review for Medical and Pharmacological Sciences
|July 8, 2020
PubMed
Abstract

Insights

Kruppel like factor 11 (KLF11) reduces oxidative stress, apoptosis, and endoplasmic reticulum stress (ERS) in osteoarthritis (OA). KLF11 protects cartilage by inhibiting the p38MAPK signaling pathway.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage breakdown.
  • Oxidative stress, apoptosis, and endoplasmic reticulum stress (ERS) are key pathological processes in OA.
  • The role of Kruppel like factor 11 (KLF11) in OA pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the effects of KLF11 on oxidative stress, apoptosis, and ERS in osteoarthritis.
  • To elucidate the underlying mechanism of KLF11's action in OA, particularly its interaction with the p38MAPK signaling pathway.

Main Methods:

  • Analysis of KLF11 expression in human articular cartilage from OA patients.
  • In vitro studies using human chondrocytes with KLF11 overexpression and IL-1β induction.
  • Investigation of the p38MAPK signaling pathway using the agonist P79350.

Main Results:

  • Elevated KLF11 expression was observed in OA cartilage and IL-1β-induced chondrocytes.
  • KLF11 overexpression significantly decreased oxidative stress, apoptosis, and ERS markers in chondrocytes.
  • Activation of the p38MAPK pathway by P79350 diminished the protective effects of KLF11.

Conclusions:

  • KLF11 exhibits a protective role in osteoarthritis by mitigating oxidative stress, apoptosis, and ERS in chondrocytes.
  • KLF11 exerts its protective effects through the inhibition of the p38MAPK signaling pathway.

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