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  2. Exploring ANT1 dysfunction as a pathological driver of wooden breast myopathy in broiler chickens

Exploring ANT1 dysfunction as a pathological driver of wooden breast myopathy in broiler chickens

  • Poult Sci. 2025 Aug 26;104(11):105730. doi: 10.1016/j.psj.2025.105730.
Bolin Zhong 1 Beibei Wang 2 Yaxing Liu 1 Di Zhao 1 Xi He 1 Zehe Song 1 Kun Xie 3
Affiliations

Affiliations

  • 1 College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China; Hunan Engineering Research Center of Poultry Production Safety, Changsha 410128, China; Yuelushan Laboratory, Changsha 410128, China.
  • 2 College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China; Hunan Engineering Research Center of Poultry Production Safety, Changsha 410128, China; Yuelushan Laboratory, Changsha 410128, China; College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China.
  • 3 College of Animal Science and Technology, Hunan Agricultural University, Changsha 410128, China; Hunan Engineering Research Center of Poultry Production Safety, Changsha 410128, China; Yuelushan Laboratory, Changsha 410128, China. Electronic address: xcl3253018@outlook.com.
Abstract

Wooden breast (WB) myopathy has become a critical quality defect in modern broiler chickens, primarily due to rapid growth driven by selective breeding. This myopathy negatively impacts the appearance, texture, and functionality of breast meat, resulting in significant economic losses to the poultry industry. The underlying pathology of WB myopathy involves metabolic dysregulation, including ATP deficits, oxidative stress, lipid metabolism imbalance, and impaired protein homeostasis. These issues are further aggravated by hypoxia, chronic inflammation, and fibrosis, leading to the characteristic muscle hardness and reduced meat quality. In this study, we evaluated adenine nucleotide translocator protein 1 (ANT1) as a key regulator of WB myopathy in severe WB samples from Arbor Acres broilers (n = 16). WB-affected muscles exhibited significant metabolic alterations, including ATP depletion, impaired fatty acid metabolism, and a metabolic shift toward glycolysis, accompanied by the upregulation of atrogin-1 and MuRF1, markers of muscle atrophy. Similarly, ANT1-deficient C2C12 cells demonstrated impaired fatty acid metabolism, reduced ATP production, and increased autophagic activity. Interestingly, while ANT1 deficiency enhanced Autophagy in vitro, WB-affected muscle tissue exhibited paradoxical Autophagy impairment, suggesting that protein degradation dysfunction in WB is not directly related to ANT1 deficiency. Further analysis revealed that enhancing Autophagy through rapamycin treatment in ANT1-deficient C2C12 cells restored ATP levels and partially rescued fatty acid metabolism. These findings, based on severe WB cases from Arbor Acres broilers at a single time point, suggest that ANT1 dysfunction may be one contributing factor to impaired autophagy-mediated muscle metabolic regeneration. However, these results should be interpreted as a preliminary piece of the broader mechanistic puzzle rather than a definitive explanation. Further studies across different severities, sampling times, and broiler strains are required before considering autophagy-targeted interventions as a viable strategy for WB mitigation.

Keywords

ANT1; Meat quality; Mitochondrial autophagy; Mitochondrial function; Muscle fiber; Wooden breast myopathy.

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