ArticleAging2021
Inhibition of complement C5a receptor protects lung cells and tissues against lipopolysaccharide-induced injury via blocking pyroptosis.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanisms and therapeutic strategies of pyroptosis in sepsis‑induced acute lung injury (Review).International journal of molecular medicine · 2026Review
- Effect of C5a Receptor Antagonist on the Osteogenic Differentiation of Dental Pulp Stem Cells.Clinical and experimental dental research · 2026Article
- Extracellular Vesicles as Drivers of Lung Endothelial Dysfunction in ARDS: Mechanisms and Therapeutic Opportunities.Comprehensive Physiology · 2026Review
- C5a/C5aR regulates Th1/Th2 imbalance in sepsis-associated lung injury by promoting neutrophil activation to increase PAD4 expression.Annals of medicine · 2025Article
- Mechanisms and Nanomedicine Interventions of Acute Lung Injury Induced by Intestinal Ischemia-Reperfusion: A Mini Review.International journal of nanomedicine · 2025Review
- Unphysiological lung strain promotes ventilation-induced lung injury via activation of the PECAM-1/Src/STAT3 signaling pathway.Frontiers in pharmacology · 2024Article
- Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- New insight of complement system in the process of vascular calcification.Journal of cellular and molecular medicine · 2023Review
- Determination of the optimal concentration and duration of C5aR antagonist application in an inflammatory model of human dental pulp cells.FEBS open bio · 2023Article
- Kindlin-2 Mediates Lipopolysaccharide-Induced Acute Lung Injury Partially via Pyroptosis in Mice.Inflammation · 2022Article
- Honokiol alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome-mediated pyroptosis via Nrf2 activation in vitro and in vivo.Chinese medicine · 2021Article
- Article
- Effect of Decay-accelerating Factor on LPS-induced Acute Lung Injury in the Rat.In vivo (Athens, Greece)Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is the injury of alveolar epithelial cells and capillary endothelial cells caused by various factors. Complement system and pyroptosis have been proved to be involved in ALI, and inhibition of C5a/C5a receptor (C5aR) could alleviate ALI. This study aimed to investigate whether C5a/C5aR inhibition could protect against LPS-induced ALI via mediating pyroptosis. Rats were assigned into four groups: Control, LPS, LPS+W-54011 1mg/kg, and LPS+W-54011 5mg/kg. Beas-2B cells pretreated with or without C5a and W-54011, alone and in combination, were challenged with LPS+ATP. Results unveiled that LPS caused lung tissue injury and inflammatory response, increased pyroptotic and apoptotic factors, along with elevated C5a concentration and C5aR expressions. However, W-54011 pretreatment alleviated lung damage and pulmonary edema, reduced inflammation and prevented cell pyroptosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.