Second-degree burns are the most common type of burn in clinical practice and hard to manage. Their treatment requires not only a consideration of the different outcomes that may arise from the dressing changes or surgical therapies themselves but also an evaluation of factors such as the burn site, patient age and burn area. Meanwhile, special attention should be given to the fact that there is no unified standard or specification for the diagnosis, classification, surgical procedure, and infection diagnosis and grading of second-degree burn wounds. This not only poses great challenges to the formulation of clinical treatment plans but also significantly affects the consistency of clinical studies. Moreover, currently, there are relatively few guidelines or expert consensus for the management of second-degree burn wounds, and no comprehensive and systematic guidelines or specifications for the treatment of second-degree burns have been formed. Therefore, we developed the Consensus on the Treatment of Second-Degree Burn Wounds (2024 edition), based on evidence-based medicine and expert opinion. This consensus provides specific recommendations on prehospital first aid, nonsurgical treatment, surgical treatment and infection treatment for second-degree burns. The current consensus generated a total of 58 recommendations, aiming to form a standardized clinical treatment plan.
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Open Access
Guideline
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Open Access
Research Article
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Sepsis-associated acute lung injury (ALI) is driven by endothelial barrier dysfunction and endothelial–mesenchymal transition (EndoMT), mediated by TGF-β1/SMAD3 signaling. Despite the therapeutic potential of SMAD3, current inhibitors face limitations. As endogenous small molecules that are closely related to physiological regulatory processes, microRNAs (miRNAs) have more potential research value for regulating SMAD3. Therefore, this study aimed to investigate the protective effect and molecular mechanism of a key miRNA targeting SMAD3 in sepsis-ALI.
Screening multiple databases revealed that miR-23b-3p was the sole miRNA targeting SMAD3. Lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) and cecal ligation/puncture (CLP) mice were used to model sepsis. Lentivirus was used to construct stable strains. The functional performance and mechanism were verified by key techniques, including dual-luciferase assays, rescue experiments, reverse transcription–quantitative polymerase chain reaction (qPCR)/Western blotting, monocyte adhesion/permeability assays, and histopathology.
In LPS-stimulated HUVECs, miR-23b-3p downregulation correlated with TGF-β1/SMAD3 activation, EndoMT progression, and barrier disruption. miR-23b-3p overexpression reversed these effects by restoring the expression of junctional proteins and suppressing the expression of mesenchymal markers. Chromatin isolation by RNA purification–qPCR, RNA pull-down, and dual-luciferase assays confirmed the direct miR-23b-3p–SMAD3 3′UTR interaction. Rescue experiments demonstrated that miR-23b-3p counteracts TGF-β1/SMAD3 hyperactivation. In CLP mice, intratracheal agomiR-23b-3p attenuated lung injury, normalized alveolar architecture, and reduced vascular leakage by suppressing endothelial Smad3 upregulation.
miR-23b-3p is a SMAD3-targeting regulator that inhibits EndoMT and repairs endothelial barrier integrity. Mechanistically, miR-23b-3p preserves endothelial homeostasis via SMAD3-dependent EndoMT inhibition. This study provides mechanistic insights and a miRNA-based therapeutic strategy for sepsis-induced ALI.
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