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In Vitro Impact Model to Generate Sublethal Chondrocyte Injury in Bovine Cartilage Explants

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Transient receptor potential channels in chondrocyte homeostasis and pathophysiology: From molecular mechanisms to

Yehong Wang1, Tingting Tian1, Caixia Yi2

  • 1Hunan Provincial Key Laboratory of Dong Medicine, Biomedical Research Institute, Hunan University of Medicine, Huaihua, 418000, PR China.

International Journal of Biological Macromolecules
|November 16, 2025
PubMed

Insights

Transient receptor potential (TRP) channels are key in osteoarthritis (OA) pathogenesis. Targeting specific TRP channels offers potential for cartilage repair and personalized OA treatments.

Area of Science:

  • Molecular Biology
  • Biochemistry
  • Cell Biology

Background:

  • Transient receptor potential (TRP) channels are crucial for chondrocyte function and cartilage health.
  • Dysregulation of TRP channels contributes significantly to osteoarthritis (OA) development and progression.
  • Understanding TRP channel roles is vital for developing effective OA therapies.

Purpose of the Study:

  • To review the multifaceted roles of TRP channel subtypes in chondrocyte biology.
  • To elucidate the mechanisms underlying TRP channel involvement in OA pathogenesis.
  • To explore the translational potential of TRP channels as therapeutic targets for OA.

Main Methods:

  • Literature review synthesizing current research on TRP channels in chondrocytes and OA.
  • Analysis of molecular mechanisms involving specific TRP subtypes (e.g., TRPV4, TRPA1, TRPM7, TRPV1).
  • Evaluation of preclinical findings for pharmacological interventions and future therapeutic strategies.

Main Results:

  • TRPV4 acts as a mechanosensor with dual roles in cartilage repair and degeneration.
  • TRPA1 exacerbates OA by promoting inflammation and matrix degradation.
  • TRPM7 and TRPV1 are implicated in maintaining chondrocyte homeostasis through calcium/magnesium regulation and ferroptosis suppression.
  • Other TRP subtypes (TRPC1, TRPV5, TRPM8) also contribute to OA pathology.
  • Pharmacological interventions show promise but face challenges in translation.

Conclusions:

  • TRP channels are critical regulators of chondrocyte homeostasis and OA pathogenesis.
  • Targeting specific TRP channels offers a promising therapeutic avenue for OA treatment.
  • Future research should focus on precision medicine approaches, including intra-articular delivery and AI-driven drug design for TRP channel modulation.
Keywords:
ChondrocytesInflammationMechanotransductionOsteoarthritisTRP channels

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