5. Conclusions
We identified a large number of hypoxia associated markers in the muscles of P. vachelli that were involved in diverse biological pathways such as HIF-1 signaling, energy metabolism, and muscle function. Compared with the P. vachelli livers, we found that muscles experienced significant hypoxia-associated changes, and this was evident in discrete tissue-specific patterns present. For example, P. vachelli livers have increased anaerobic glycolysis, heme synthesis, erythropoiesis, and inhibited apoptosis when exposed to under 4 h of hypoxia, whereas the opposite was true to muscles.
To maintain normal physical activity, fishes acutely react to acute hypoxia, by activated catabolic pathways to generate more energy, decreased biosynthesis to reduce energy consumption, and shifted from aerobic to anaerobic metabolic contributions. We found that hypoxia induced muscle dysfunction through impairing mitochondrial function, activating inflammasome, and apoptosis (Zhou et al. 2011). The hypoxia-induced mitochondrial dysfunction enhanced ROS generation and apoptosis, further triggering IL-1β production via the inflammasome activation (Pomerantz et al.2001). In turn, IL-1β further impaired mitochondrial function and apoptosis by suppressing downstream mitochondrial biosynthesis related proteins, resulting in a vicious circle between inflammasome activation and mitochondrial dysfunction (Yi et al. 2015) (Fig. 7 ). We hope that it provides fundamental data on analytical methods, as well as biological and mechanical insights into future research for environmental stress induced hypoxia.