Klf10 is involved in extracellular matrix calcification of chondrocytes alleviating chondrocyte senescence

J Transl Med. 2024 Jan 13;22(1):52. doi: 10.1186/s12967-023-04666-7.

Abstract

Osteoarthritis (OA) is a chronic degenerative disease resulting joint disability and pain. Accumulating evidences suggest that chondrocyte extracellular matrix calcification plays an important role in the development of OA. Here, we showed that Krüppel-like factor 10 (Klf10) was involved in the regulation of chondrocyte extracellular matrix calcification by regulating the expression of Frizzled9. Knockdown of Klf10 attenuated TBHP induced calcification and reduced calcium content in chondrocytes. Restoring extracellular matrix calcification of chondrocytes could aggravate chondrocyte senescence. Destabilization of a medial meniscus (DMM) mouse model of OA, in vivo experiments revealed that knockdown Klf10 improved the calcification of articular cartilage and ameliorated articular cartilage degeneration. These findings suggested that knockdown Klf10 inhibited extracellular matrix calcification-related changes in chondrocytes and alleviated chondrocyte senescence.

MeSH terms

  • Animals
  • Calcinosis* / genetics
  • Cartilage, Articular* / metabolism
  • Chondrocytes / metabolism
  • Extracellular Matrix / metabolism
  • Mice
  • Osteoarthritis* / genetics

Substances

  • KLF10 protein, mouse