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Formyl peptide receptor 2 (FPR2) mediates cisplatin-induced cochlear inflammation and hair cell apoptosis

Jiaojiao Hou1, Rui Liang2, Yuhan Lin1

  • 1Department of Physiology, Jinzhou Medical University, Jinzhou 121000, China.

Toxicology
|July 6, 2025
PubMed

Insights

Formyl peptide receptor 2 (FPR2) drives cisplatin-induced hearing loss by promoting inflammation and hair cell death. Inhibiting FPR2 significantly protects against this ototoxicity, offering a potential therapeutic target.

Area of Science:

  • Ototoxicity research
  • Cancer therapeutics
  • Molecular biology

Background:

  • Cisplatin is an effective chemotherapy drug but causes significant hearing loss (ototoxicity).
  • The precise mechanisms behind cisplatin-induced ototoxicity remain unclear.
  • Formyl peptide receptor 2 (FPR2) is a G protein-coupled receptor implicated in inflammatory responses.

Purpose of the Study:

  • To investigate the role of FPR2 in cisplatin-induced ototoxicity.
  • To explore FPR2 as a potential therapeutic target for preventing cisplatin-induced hearing loss.

Main Methods:

  • Upregulation of FPR2 in mouse cochlea post-cisplatin exposure was assessed.
  • Genetic (knockdown) and pharmacological (Boc-2 antagonist) methods were used to block FPR2.
  • Auditory brainstem response (ABR) thresholds were measured in mice.
  • ERK1/2 and NF-κB signaling pathways were analyzed.
  • Pro-inflammatory cytokine release and hair cell apoptosis were evaluated.

Main Results:

  • Cisplatin exposure significantly upregulated FPR2 in the cochlea, correlating with hearing loss.
  • Blocking FPR2 with Boc-2 or genetic knockdown mitigated cisplatin-induced hearing impairment.
  • FPR2 activation was shown to trigger ERK1/2 and NF-κB pathways, leading to inflammation and hair cell apoptosis.
  • FPR2 inhibition reduced inflammatory markers and hair cell death.

Conclusions:

  • FPR2 is a key mediator of cisplatin-induced ototoxicity.
  • Targeting FPR2 presents a promising strategy for preventing chemotherapy-induced hearing loss in cancer patients.
Keywords:
ApoptosisCisplatinCochleaFormyl peptide receptor 2Inflammation

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