This analysis reveals distinct transcriptomic adaptations in heart and liver under heat stress, suggesting metabolism and cytokine signaling adaptations.
Heat stress (HS) poses a significant threat to poultry production, impairing growth, metabolism, and survival. This study investigates the transcriptomic responses of broiler heart and liver tissues to acute (2h, 38°C) and chronic (6h, 38°C) HS, revealing distinct and shared molecular adaptations. Differential gene expression (DEG) analysis identified more pronounced transcriptomic changes under chronic HS (heart: 2,503 DEGs; liver: 2,236 DEGs) compared to acute HS (heart: 1,217 DEGs; liver: 1,843 DEGs). Shared DEGs (1,193 genes) included heat shock proteins (HSP90AA1, HSPA4, HSPB8), antioxidants (GPX1), and structural regulators (CSRP3, MYOZ3), indicating conserved stress responses. Tissue-specific patterns emerged: the heart emphasized cytokine signaling and protein folding, while the liver exhibited metabolic suppression and cytoskeletal remodeling. Weighted gene co-expression network analysis (WGCNA) highlighted stress-duration-dependent modules, with liver modules linked to metabolism and heart modules to immune and redox regulation. Temporal clustering revealed dynamic expression shifts, with chronic HS enhancing protein chaperone activity and acute HS triggering rapid signaling adjustments. These findings elucidate key molecular mechanisms underlying HS adaptation, offering potential targets for improving poultry thermotolerance through nutritional or genetic strategies.
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Yang et al. (2025) studied this question.
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