摘要
Obesity is a chronic disease caused by an excess of adipose tissue that may impair health by altering the functionality of various organs, including the lungs. Excessive deposition of fat in the abdominal area can lead to abnormal positioning of the diaphragm and consequent reduction in lung volume, leading to a heightened demand for ventilation and increased exposure to respiratory diseases, such as chronic obstructive pulmonary disease, asthma, and obstructive sleep apnoea. In addition to mechanical ventilatory constraints, excess fat and ectopic deposition in visceral depots can lead to adipose tissue dysfunction, which promotes metabolic disorders. An altered adipokine-secretion profile from dysfunctional adipose tissue in morbid obesity fosters systemic, low-grade inflammation, impairing pulmonary immune response and promoting airway hyperresponsiveness. A potential target of these adipokines could be the NLRP3 inflammasome, a critical component of the innate immune system, the harmful pro-inflammatory effect of which affects both adipose and lung tissue in obesity. In this review, we will investigate the crosstalk between adipose tissue and the lung in obesity, highlighting the main inflammatory mediators and novel therapeutic targets in preventing pulmonary dysfunction.
摘要译文
肥胖是一种慢性疾病，由过量的脂肪组织引起，可能通过改变包括肺在内的各种器官的功能来损害健康。腹部脂肪的过度沉积会导致隔膜异常定位，从而减少肺部体积，从而导致通风的需求增强和增加呼吸道疾病的暴露，例如慢性阻塞性肺部疾病，哮喘和阻塞性睡眠呼吸暂停。除了机械通气的约束外，内脏库中过多的脂肪和异位沉积还会导致脂肪组织功能障碍，从而促进代谢性疾病。病态肥胖症中功能失调的脂肪组织的脂肪因子分泌谱改变了系统性，低度炎症，损害肺免疫反应并促进气道高反应性。这些脂肪因子的潜在靶标可能是NLRP3炎性体，这是先天免疫系统的关键成分，它的有害促炎作用会影响肥胖症中脂肪和肺组织。在这篇综述中，我们将研究肥胖症中脂肪组织与肺之间的串扰，从而突出主要的炎症介质和新的治疗靶标，以防止肺功能障碍。
Giuseppe Palma;Gian Pio Sorice;Valentina Annamaria Genchi;Fiorella Giordano;Cristina Caccioppoli;Rossella D’Oria;Nicola Marrano;Giuseppina Biondi;Francesco Giorgino;Sebastio Perrini. Adipose Tissue Inflammation and Pulmonary Dysfunction in Obesity[J]. International Journal of Molecular Sciences, 2022,23(13): 7349