Cetaceans face compounding threats from diverse anthropogenic activities, including vessel strikes, entanglement, and pollution. However, these stressors have predominantly been assessed in isolation, overlooking the potential synergistic effects arising from their frequent co-occurrence. Polybrominated diphenyl ethers (PBDEs), a class of toxic flame retardants ubiquitous in marine environments, bioaccumulate in cetaceans posing significant health risks. This study provides the first integrated mechanistic insight into how PBDE exposure not only directly compromises cetacean health but also amplifies the impacts of other anthropogenic pressures. Specifically, we demonstrate that PBDE exposure delays wound healing in cetaceans by impairing skin fibroblast migration. Further analysis reveals that PBDEs significantly downregulate Type I and Type VI collagen expression and suppress the promotive effect of TGF-β1 on cell transition by enhancing SMAD2 phosphorylation, thus disrupting extracellular matrix (ECM) expression and impeding cellular migration. Our findings demonstrate that PBDEs impair wound healing in cetaceans by disrupting ECM remodeling through dual inhibition of collagen homeostasis and the TGF-β1/Smad signaling pathway. Considering that risk of injuries is increasing due to increase in fishing and transportation vessels, the delayed wound healing induced by pollutants such as PBDEs may increase mortality in cetacean populations.
 

Cetacean,,wound