Sun Xutao, Mao Caiyun, Wang Jiaxin, Wu Siyu, Qu Ying, Xie Ying, Sun Fengqi, Jiang Deyou, Song Yunjia
Department of Typhoid, School of Basic Medical Sciences, Heilongjiang University of Chinese Medicine, Harbin 150040, China.
Department of Pharmacology, School of Basic Medical Sciences, Heilongjiang University of Chinese Medicine, Harbin 150040, China.
Curr Issues Mol Biol. 2024 Jul 7;46(7):7147-7168. doi: 10.3390/cimb46070426.
Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), are pulmonary conditions that cause significant morbidity and mortality. The common etiologies of these conditions include pneumonia, pulmonary contusion, fat embolism, smoke inhalation, sepsis, shock, and acute pancreatitis. Inflammation, oxidative stress, apoptosis, and autophagy are key pathophysiological mechanisms underlying ALI. Hydrogen sulfide (HS) and sulfur dioxide (SO) are sulfur-containing gas signaling molecules that can mitigate these pathogenic processes by modulating various signaling pathways, such as toll-like receptor 4 (TLR4)/nod-like receptor protein 3 (NLRP3), extracellular signal-regulating protein kinase 1/2 (ERK1/2), mitogen-activated protein kinase (MAPK), phosphatidyl inositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), and nuclear factor kappa B (NF-κB), thereby conferring protection against ALI. Given the limited clinical effectiveness of prevailing ALI treatments, investigation of the modulation of sulfur-containing gas signaling molecules (HS and SO) in ALI is imperative. This article presents an overview of the regulatory pathways of sulfur-containing gas signaling molecules in ALI animal models induced by various stimuli, such as lipopolysaccharide, gas inhalation, oleic acid, and ischemia-reperfusion. Furthermore, this study explored the therapeutic prospects of diverse HS and SO donors for ALI, stemming from diverse etiologies. The aim of the present study was to establish a theoretical framework, in order to promote the new treatment of ALI.
急性肺损伤（ALI）及其最严重的形式急性呼吸窘迫综合征（ARDS）是导致显著发病率和死亡率的肺部疾病。这些病症的常见病因包括肺炎、肺挫伤、脂肪栓塞、烟雾吸入、败血症、休克和急性胰腺炎。炎症、氧化应激、细胞凋亡和自噬是ALI潜在的关键病理生理机制。硫化氢（HS）和二氧化硫（SO）是含硫气体信号分子，可通过调节各种信号通路（如Toll样受体4（TLR4）/NOD样受体蛋白3（NLRP3）、细胞外信号调节蛋白激酶1/2（ERK1/2）、丝裂原活化蛋白激酶（MAPK）、磷脂酰肌醇3激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素哺乳动物靶蛋白（mTOR）和核因子κB（NF-κB））来减轻这些致病过程，从而对ALI起到保护作用。鉴于现行ALI治疗的临床效果有限，研究含硫气体信号分子（HS和SO）在ALI中的调节作用势在必行。本文概述了在由脂多糖、气体吸入、油酸和缺血再灌注等各种刺激诱导的ALI动物模型中含硫气体信号分子的调节途径。此外，本研究探讨了不同来源的HS和SO供体对ALI的治疗前景。本研究的目的是建立一个理论框架，以推动ALI的新治疗方法。
