1 Department of Respiratory Medicine, Laboratory for Translational Research in Obstructive Pulmonary Diseases, Ghent University Hospital, Ghent, Belgium.
2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, and.
Am J Respir Cell Mol Biol. 2019 Jun;60(6):621-628. doi: 10.1165/rcmb.2018-0379TR.
GDF-15 (growth differentiation factor 15) acts both as a stress-induced cytokine with diverse actions at different body sites and as a cell-autonomous regulator linked to cellular senescence and apoptosis. For multiple reasons, this divergent transforming growth factor-β molecular superfamily member should be better known to pulmonary researchers and clinicians. In ambulatory individuals, GDF-15 concentrations in peripheral blood are an established predictive biomarker of all-cause mortality and of adverse cardiovascular events. Concentrations upon admission of critically ill patients (without or with sepsis) correlate with organ dysfunction and independently predict short- and long-term mortality risk. GDF-15 is a major downstream mediator of p53 activation, but it can also be induced independently of p53, notably by nonsteroidal antiinflammatory agents. GDF-15 blood concentrations are markedly elevated in adults and children with pulmonary hypertension. Concentrations are also increased in chronic obstructive pulmonary disease, in which they contribute to mucus hypersecretion, airway epithelial cell senescence, and impaired antiviral defenses, which together with murine data support a role for GDF-15 in chronic obstructive pulmonary disease pathogenesis and progression. This review summarizes biological and clinical data on GDF-15 relevant to pulmonary and critical care medicine. We highlight the recent discovery of a central nervous system receptor for GDF-15, GFRAL (glial cell line-derived neurotrophic factor family receptor-α-like), an important advance with potential for novel treatments for obesity and cachexia. We also describe limitations and controversies in the existing literature, and we delineate research questions that must be addressed to determine whether GDF-15 can be therapeutically manipulated in other clinical settings.
GDF-15(生长分化因子 15)既是一种应激诱导的细胞因子,在不同的身体部位具有多种作用,也是一种与细胞衰老和凋亡相关的细胞自主调节因子。出于多种原因,这种具有不同转化生长因子-β分子超家族成员的因子应该为肺部研究人员和临床医生所熟知。在非卧床个体中,外周血中的 GDF-15 浓度是全因死亡率和不良心血管事件的既定预测生物标志物。危重症患者(无论是否伴有败血症)入院时的浓度与器官功能障碍相关,并独立预测短期和长期死亡率风险。GDF-15 是 p53 激活的主要下游介质,但它也可以独立于 p53 诱导,特别是通过非甾体抗炎药。GDF-15 是肺动脉高压成人和儿童血液中的主要下游介质。在慢性阻塞性肺疾病中,其浓度也会升高,在慢性阻塞性肺疾病中,其浓度升高会导致黏液过度分泌、气道上皮细胞衰老和抗病毒防御受损,这些与小鼠数据一起支持 GDF-15 在慢性阻塞性肺疾病发病机制和进展中的作用。本综述总结了与肺部和重症监护医学相关的 GDF-15 的生物学和临床数据。我们强调了最近发现的 GDF-15 的中枢神经系统受体 GFRAL(神经胶质细胞衍生神经营养因子家族受体-α样),这是一个重要的进展,可能为肥胖症和恶病质的新型治疗方法提供了可能。我们还描述了现有文献中的局限性和争议,并描述了必须解决的研究问题,以确定是否可以在其他临床环境中对 GDF-15 进行治疗性干预。