Broiler ascites syndrome is a common and complex disease in broiler farming, which severely impacts broiler growth performance and health and brings huge economic losses to the breeding industry. Hypoxia has been shown to be an important cause of this disease. Prolonged exposure of broiler chickens to a hypoxic environment induces pulmonary vasoconstriction, which leads to an increase in pulmonary artery pressure, triggering pulmonary artery remodelling and compensatory right ventricular hypertrophy, and ultimately ascites. Pulmonary artery remodelling is a process in which the vascular wall tissue structure and function undergo pathological changes after the pulmonary artery is stimulated by various injuries or hypoxia, including endothelial dysfunction, abnormal proliferation of pulmonary artery smooth muscle cells, vascular fibrosis, etc. When these cells are damaged or stimulated, they may undergo programmed cell death, an orderly and regulated mode of cell death that is important for maintaining the stability of the body's internal environment. It has been demonstrated that death modes such as apoptosis and autophagy are involved in the pathophysiologic process of pulmonary hypertension, but their specific molecular mechanisms are still unclear. In this review, we first describe the pathogenesis of broiler ascites, then describe the specific mechanism of dysfunction of pulmonary artery vascular cells in broiler ascites syndrome, and finally elaborate the progression of different programmed cell death in broiler pulmonary hypertension. This study aims to elucidate the specific mechanisms underlying the dysfunction of pulmonary artery vascular cells in broiler pulmonary hypertension, thereby enhancing our understanding of the pathogenesis of this syndrome.
Keywords: Broiler ascites syndrome; hypoxia; programmed cell death; pulmonary artery endothelial cells; pulmonary artery fibroblasts; pulmonary artery remodelling; pulmonary artery smooth muscle cells.