Regulatory Role of Apoptotic and Inflammasome Related Proteins and Their Possible Functional Aspect in Thiram Associated Tibial Dyschondroplasia of Poultry

Simple Summary Tibial dyschondroplasia (TD) is a metabolic disorder that impairs bony and cartilage processes. It is common in broilers due to the consumption of thiram, especially in the industrial and agriculture zones. During the condition, cartilage does not only seem to develop ossification during its occurrence but also causes lameness, mortality, and moral convictions in commercial poultry. Moreover, it has been characterized as an economically significant condition since it causes carcass damage due to the involvement of different biological pathways that lead to a particular change in the chondrocytes. These entire cellular pathways are interconnected through various cellular inputs, including anti-apoptotic, pro-apoptotic, and executioner caspases that modulate the other essential chondrogenic proteins (collagen and aggrecan), extracellular metalloproteinases, and NLRP3 base inflammasome. Tibial dyschondroplasia debilities apoptotic and inflammasomal conditions that can further destroy chondrocytes. Inflammasomes are specialized protein complexes that process pro-inflammatory cytokines, e.g., interleukin-1 beta (IL-1 beta) and IL-18. Moreover, there is mounting evidence that many of the signaling molecules that govern programmed cell death also affect inflammasome activation in a cell-intrinsic way. During the last decade, apoptotic functions have been described for signaling molecules involving inflammatory responses and cell death pathways. Considering these exceptional developments in the knowledge of processes, this review gives a glimpse of the significance of these two pathways and their connected proteins in tibial dyschondroplasia. The current review deeply elaborates on the elevated level of signaling mediators of mitochondrial-mediated apoptosis and the inflammasome. Although investigating these pathways' mechanisms has made significant progress, this review identifies areas where more study is especially required. It might lead to developing innovative therapeutics for tibial dyschondroplasia and other associated bone disorders, e.g., osteoporosis and osteoarthritis, where apoptosis and inflammasome are the significant pathways.