GAB1 alleviates septic lung injury by inhibiting the TLR4/ NF‐κB pathway

Abstract

Sepsis is a systemic disease caused by bacterial or viral infections. SARS-COV-2, which is still rampant around the world at the end of 2019, can also cause severe viral sepsis. 1,2 Acute lung injury (ALI) is one of the most common complications of sepsis, which can lead to acute respiratory distress syndrome (ARDS) with high mortality. 3 Acute lung injury in sepsis is related to increased pulmonary vascular permeability, alveolar epithelial cell damage, and lung immune inflammatory cell activation and infiltration caused by a large number of inflammatory factors and other substances released during sepsis. 4 However, at present, the pathogenesis of acute lung injury in sepsis has not been fully studied and there is no specific drug treatment.Inflammation disorder is closely related to the pathogenesis of acute lung injury, 5 mainly related to the large release of pro-inflammatory factors and the imbalance of inflammatory factors. 6 Toll-like receptor 4 (TLR4) can specifically recognise

RETRACTED: Macrophage SAMSN1 protects against sepsis-induced acute lung injury in mice

“…Moreover, Wang et al showed that alveolar epithelium-specific GAB1 knockout perturbed surfactant homeostasis and predisposed mice to LPS-induced ALI [ 48 ]. In contrast, GAB1 overexpression dramatically reduced LPS-induced inflammation and apoptosis, thereby alleviating LPS-induced ALI in mice [ 53 ]. von Holleben et al previously identified GAB1 was a potential binding partner of SAMSN1 using BLAST data based search with its SH3 domain [ 22 ].…”

Gab1 Overexpression Alleviates Doxorubicin-Induced Cardiac Oxidative Stress, Inflammation, and Apoptosis Through PI3K/Akt Signaling Pathway

“…In the present study, we, for the first time, reported that cardiac Gab1 overexpression could inhibit DOX-induced ROS, inflammatory response, and apoptosis, which was similar to what was previously reported. 25–27…”

“…They found that Gab1 expression was markedly decreased after LPS stimulation, and Gab1 overexpression significantly decreased levels of macrophages, neutrophils, and inflammatory factors caused by LPS in bronchoalveolar lavage fluid. 27 Combining the above clues, Gab1 may be an upstream mediator of cardiac ROS, apoptosis, and inflammation induced by several pathological stimuli. However, there is no available data about the role of Gab1 in DOX-induced ROS, apoptosis, and inflammation.…”

“…In the present study, we, for the first time, reported that cardiac Gab1 overexpression could inhibit DOX-induced ROS, inflammatory response, and apoptosis, which was similar to what was previously reported. [25][26][27] It is well known that Gab1 functions downstream of various receptors of growth factors and cytokines, mediating several signaling pathways, including PI3K/Akt signaling. 29 Tyrosine kinases phosphorylate Gab1, and then phosphorylated Gab1 recruits and activates PI3K/Akt.…”