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February 3, 2024International ImmunopharmacologyOpen Access

GTS-21 attenuates ACE/ACE2 ratio and glycocalyx shedding in lipopolysaccharide-induced acute lung injury by targeting macrophage polarization derived ADAM-17

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Key result

GTS-21 alleviates acute lung injury by reducing ACE/ACE2 ratio and glycocalyx shedding via ADAM-17 inhibition.

Why the study?

GTS-21 is promising for treating LPS-induced acute lung injury, but the precise underlying mechanism remains unknown.

Population

Mouse models of ALI and AT2s injury

Comparison

GTS-21 vs LPS alone, with or without recombinant ADAM-17 or siRNA ADAM-17

Design

In vivo and in vitro preclinical study

Authors

WZWeiwei ZhuFWFengyun WangCHChang Hu

Discussion

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Member takes

Overview

Hypothesis-generating in animal ALI models; leaves open translation to human acute lung injury.

Structured PICO

P
Population
Mouse models of acute lung injury (ALI) and alveolar epithelial type II cells (AT2s) injury following treatment with lipopolysaccharides (LPS)
I
Intervention
GTS-21 (selective alpha7 nicotinic acetylcholine receptor agonist)
C
Comparator
LPS group (without GTS-21)
O
Outcome
Pathological changes, pulmonary edema, and lung compliancesurrogate

GTS-21 demonstrates protective effects against LPS-induced acute lung injury in preclinical models by modulating macrophage polarization and reducing the ACE/ACE2 ratio and glycocalyx shedding.

Cite This Study

Zhu et al. (2024) studied Acute lung injury (ALI). GTS-21 vs. LPS group was evaluated on Pathological alterations, lung permeability, inflammatory response, ACE/ACE2 ratio, and glycocalyx shedding. GTS-21 alleviated LPS-induced acute lung injury by attenuating the ACE/ACE2 ratio and glycocalyx shedding through the inhibition of macrophage M1 polarization-derived ADAM-17.

synapsesocial.com/papers/6aa91c5ae854006b655acacbhttps://doi.org/10.1016/j.intimp.2024.111603
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