Publications by authors named "Qiong-Feng Chen"

Acute liver injury (ALI) is a disease that seriously threatens human health and life, and a dysregulated inflammation response is one of the main mechanisms of ALI induced by various factors. Phosphatidylethanolamine binding protein 4 (PEBP4) is a secreted protein with multiple biological functions. At present, studies on PEBP4 exist mainly in the field of tumors and rarely in inflammation.

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Phosphatidylethanolamine-binding protein 4 (PEBP4) has been found to be highly expressed in many tumors and to be closely related to the proliferation, differentiation, and metastasis of tumors. PEBP4 has also been found to be involved in many cancer-activated signaling pathways and to cause therapeutic resistance. In this study, we first reviewed the morphological structure and expression of PEBP4, then discussed the roles of PEBP4 in individualized treatment of some cancers, and finally explored the possibilities of cultivating PEBP4 as a therapeutic target.

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Background: The renin angiotensin-aldosterone system (RAAS) and lipoxins (LXs) have similar roles in many processes. We previously reported that BML-111, a Lipoxin receptor agonist, inhibited chronic injury hepatic fibrosis by regulating RAAS, but whether LXs are involved in BML-111-mediated protection from acute injury is unclear still.

Methods: We established models of acute liver/lung injury and confirmed them with histopathology and myeloperoxidase (MPO) measurements.

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Article Synopsis
  • Previous studies suggest that lipoxin A4 (LXA4) and the ACE2-Ang-(1-7)-Mas signaling pathway have protective effects in acute lung injury (ALI), but direct evidence was lacking.
  • In this study using an LPS-induced ALI mouse model, LXA4 was shown to improve ALI outcomes by enhancing ACE2 activity and increasing levels of Ang-(1-7) and its receptor Mas.
  • LXA4 also reduced inflammation markers and inhibited the NF-κB signaling pathway, indicating its protective role in lung injury via the ACE2-Ang-(1-7)-Mas axis, with specific inhibitors reversing these beneficial effects.
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