The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury DOI Creative Commons

Shilei Cheng,

Yufei Li, Xiaoliang Sun

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Dec. 6, 2024

Acute lung injury (ALI) is a prevalent and critical complication of sepsis, marked by high incidence mortality rates, with its pathogenesis still not being fully elucidated. Recent research has revealed significant correlation between the metabolic reprogramming glucose sepsis-associated ALI (S-ALI). Throughout course S-ALI, immune cells, including macrophages dendritic undergo shifts to accommodate intricate demands function that emerge as sepsis advances. Indeed, in S-ALI serves double-edged sword, fueling inflammatory responses initial stages subsequently initiating anti-inflammatory disease evolves. In this review, we delineate current progress concerning pathogenic mechanisms linked focus on pertinent cells implicated. We encapsulate impact onset, progression, prognosis S-ALI. Ultimately, examining key regulatory factors within intermediates enzymes, have identified potential therapeutic targets reprogramming, striving tackle inherent challenges diagnosing treating Severe Lung Injury (S-ALI) greater efficacy.

Language: Английский

Anti-Inflammatory Potential of the Anti-Diabetic Drug Metformin in the Prevention of Inflammatory Complications and Infectious Diseases Including COVID-19: A Narrative Review DOI Open Access

Trevor J. Plowman,

Hannah Christensen,

Myia Aiges

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(10), P. 5190 - 5190

Published: May 10, 2024

Metformin, a widely used first-line anti-diabetic therapy for the treatment of type-2 diabetes, has been shown to lower hyperglycemia levels in blood by enhancing insulin actions. For several decades this drug globally successfully control hyperglycemia. Lactic acidosis be major adverse effect metformin some diabetic patients, but studies suggest that it is typically well-tolerated and safe most patients. Further, recent also indicate its potential reduce symptoms associated with various inflammatory complications infectious diseases including coronavirus disease 2019 (COVID-19). These besides could as an adjuvant diseases. In article, we discuss current understanding role prevention both diabetics non-diabetics.

Language: Английский

Citations

8
Pyruvate kinase M2 modulates mitochondrial dynamics and EMT in alveolar epithelial cells during sepsis-associated pulmonary fibrosis DOI Creative Commons

Jinhua Feng,

Xi Huang, Yawen Peng

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 19, 2025

Language: Английский

Citations

0
PGC-1α mediates migrasome secretion accelerating macrophage–myofibroblast transition and contributing to sepsis-associated pulmonary fibrosis DOI Creative Commons
Yawen Peng, Shuya Mei,

Xiaohui Qi

et al.

Experimental & Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Abstract Sepsis-associated pulmonary fibrosis (SAPF) is a critical pathological stage in the progression of sepsis-induced acute respiratory distress syndrome. While aggregation and activation lung fibroblasts are central to initiation fibrosis, macrophage–myofibroblast transition (MMT) has recently been identified as novel source this context. However, mechanisms driving MMT remain inadequately understood. Given emerging role migrasomes (novel extracellular vesicles mediating intercellular communication), we investigated their involvement fibrosis. Here utilized lipopolysaccharide-induced SAPF mouse model an vitro co-culture system macrophages observe process during SAPF. We found that lipopolysaccharide exposure suppresses PGC-1α expression fibroblasts, resulting mitochondrial dysfunction accumulation cytosolic DNA (mtDNA). This promotes secretion mtDNA-containing migrasomes, which, turn, initiate contribute progression. Notably, mitigates dysfunction, reduces mtDNA-migrasome release, inhibits alleviates In conclusion, our study identifies suppression subsequent release mtDNA mechanism These findings suggest targeting crosstalk between immune cells mediated by could represent promising therapeutic strategy for

Language: Английский

Citations

0
LPS-induced monocarboxylate transporter-1 inhibition facilitates lactate accumulation triggering epithelial-mesenchymal transformation and pulmonary fibrosis DOI Creative Commons

Jinhua Feng,

Han Zhong,

Shuya Mei

et al.

Cellular and Molecular Life Sciences, Journal Year: 2024, Volume and Issue: 81(1)

Published: May 6, 2024

Abstract The epithelial-mesenchymal transformation (EMT) process of alveolar epithelial cells is recognized as involved in the development pulmonary fibrosis. Recent evidence has shown that lipopolysaccharide (LPS)-induced aerobic glycolysis lung tissue and elevated lactate concentration are associated with pathogenesis sepsis-associated However, it uncertain whether LPS promotes fibrosis by promoting accumulation tissue, thereby initiating EMT process. We hypothesized monocarboxylate transporter-1 (MCT1), main protein for transport, may be crucial pathogenic found high concentrations induced while moderate did not. Besides, we demonstrated MCT1 inhibition enhanced MLE-12 cells, upregulation could reverse lactate-induced EMT. promote through accumulation, this alleviated upregulating expression MCT1. In addition, overexpression prevented LPS-induced vivo. Altogether, study revealed inhibit mouse cause transport disorder, which leads to ultimately

Language: Английский

Citations

3
Sinomenine ameliorates bleomycin-induced pulmonary fibrosis by inhibiting the differentiation of fibroblast into myofibroblast DOI Creative Commons

Zuqiong Nie,

Jing Wu,

Jun Xie

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(13), P. e33314 - e33314

Published: June 24, 2024

Language: Английский

Citations

0
The impact of glucose metabolism on inflammatory processes in sepsis-induced acute lung injury DOI Creative Commons

Shilei Cheng,

Yufei Li, Xiaoliang Sun

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Dec. 6, 2024

Acute lung injury (ALI) is a prevalent and critical complication of sepsis, marked by high incidence mortality rates, with its pathogenesis still not being fully elucidated. Recent research has revealed significant correlation between the metabolic reprogramming glucose sepsis-associated ALI (S-ALI). Throughout course S-ALI, immune cells, including macrophages dendritic undergo shifts to accommodate intricate demands function that emerge as sepsis advances. Indeed, in S-ALI serves double-edged sword, fueling inflammatory responses initial stages subsequently initiating anti-inflammatory disease evolves. In this review, we delineate current progress concerning pathogenic mechanisms linked focus on pertinent cells implicated. We encapsulate impact onset, progression, prognosis S-ALI. Ultimately, examining key regulatory factors within intermediates enzymes, have identified potential therapeutic targets reprogramming, striving tackle inherent challenges diagnosing treating Severe Lung Injury (S-ALI) greater efficacy.

Language: Английский

Citations

0