Wooden Breast is a myopathy affecting broiler chickens, characterized by hardening of the pectoral muscle, fibrosis, adipogenesis, and deteriorated meat quality. This study investigated the pathological mechanisms underlying wooden breast development, focusing on the interplay between fibrogenesis and myogenesis. Seventy-eight broiler chickens were categorized into normal, mild, and severe wooden breast groups based on the extent of fibrosis and adipogenesis in the pectoral muscle. Histological analysis revealed immature collagen fibers within muscle fascicles in severe wooden breast, indicating concurrent fibrogenesis and muscle regeneration. Immunofluorescence staining confirmed the close spatial localization of fibro-adipogenic progenitors (FAPs) and myosatellite cells in these areas, suggesting potential interaction during wooden breast pathogenesis. RNA sequencing and qPCR revealed upregulation of PAX7 and MYOG, markers of myogenesis, in the affected pectoral muscle, whereas MYOD expression remained unchanged. This pattern indicates an attempt at myogenic differentiation that is ultimately disrupted in severe wooden breast samples. Furthermore, cellular communication network (CCN) family members, particularly CCN2 and CCN4, were upregulated in the wooden breast-affected pectoral muscle. CCN4 expression strongly correlated with the fibro-adipogenic progenitor marker PDGFRα, implying that fibro-adipogenic progenitors-mediated CCN4 secretion contributes to wooden breast pathogenesis. Our findings suggest that fibro-adipogenic progenitors and cellular communication network family members are associated with an imbalance between fibrogenesis and myogenesis, leading to the muscle degeneration observed in wooden breast.
Kobayashi et al. (Thu,) studied this question.