Proanthocyanidins attenuates ferroptosis against influenza-induced acute lung injury in mice by reducing IFN-γ

Lv, Yiwen; Du, Youwei; Ma, Shengsuo; Shi, Yucong; Xu, Huachong; Deng, Li; Chen, Xiaoyin

doi:10.1016/j.lfs.2022.121279

Cited by 19 publications

(6 citation statements)

References 39 publications

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“…In this study, we also found that exposure to disinfectants can be linked to various types of chronic diseases including cancer, autoimmune disease, cardiovascular disease, and neurodegenerative disease. Furthermore, accumulated evidence has suggested that SLC7A11, IL-11, and IL-24 are closely associated with the development of chronic pulmonary diseases ( Rao et al, 2021 ; Fung et al, 2022 ; Park et al, 2022 ; Lv et al, 2023 ). Therefore, we suggest that detailed studies are needed to clarify our hypothesis and to set a strategy for the effective application (including the acceptable concentration of each ingredient in products for continued safe use).…”

Section: Discussionmentioning

confidence: 99%

Comparison of disinfectants-induced gene expression profile: Potential adverse effects

Park

Jin

Shim

et al. 2023

Toxicology and Applied Pharmacology

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Section: Discussionmentioning

confidence: 99%

Comparison of disinfectants-induced gene expression profile: Potential adverse effects

Park

Jin

Shim

et al. 2023

Toxicology and Applied Pharmacology

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“…This is called the arachidonic acid remodeling pathway, where ACSL4 plays a pivotal role. Interestingly, the protein expression of ACSL4 has been reported to be induced by the infection with SARS-CoV-2 and influenza virus 34 , 35 , which may explain an increase in PE-20:4 and PE-22:6 reported in the plasma of COVID-19 patients 36 in addition to that in PE-20:4, PE-22:6, PC-20:4, and PC-22:6 in influenza studies 23 in animal models including the present study. Clinical studies on patients with Ebola and zika virus infectious diseases also reported elevated PE-PUFA including PE-20:4 and PE-22:6, but not PC-PUFA 37 , 38 .…”

Section: Discussionmentioning

confidence: 99%

The elucidation of plasma lipidome profiles during severe influenza in a mouse model

Ohno,

Gowda,

Sekiya

et al. 2023

Sci Rep

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Although influenza virus infection has been shown to affect lipid metabolism, details remain unknown. Therefore, we elucidated the kinetic lipid profiles of mice infected with different doses of influenza virus A/Puerto Rico/8/34 (H1N1) (PR8) by measuring multiple lipid molecular species using untargeted lipidomic analysis. C57BL/6 male mice were intranasally infected with PR8 virus at 50 or 500 plaque-forming units to cause sublethal or lethal influenza, respectively. Plasma and tissue samples were collected at 1, 3, and 6 days post-infection (dpi), and comprehensive lipidomic analysis was performed using high-performance liquid chromatography–linear trap quadrupole–Orbitrap mass spectrometry, as well as gene expression analyses. The most prominent feature of the lipid profile in lethally infected mice was the elevated plasma concentrations of phosphatidylethanolamines (PEs) containing polyunsaturated fatty acid (PUFA) at 3 dpi. Furthermore, the facilitation of PUFA-containing phospholipid production in the lungs, but not in the liver, was suggested by gene expression and lipidomic analysis of tissue samples. Given the increased plasma or serum levels of PUFA-containing PEs in patients with other viral infections, especially in severe cases, the elevation of these phospholipids in circulation could be a biomarker of infection and the severity of infectious diseases.

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“…Clinically, the main symptoms are decreased lung compliance and bilateral pulmonary inflammatory infiltrates in hypoxemia ( 104 ). Ferroptosis is the main driver of ischemia-reperfusion injury (I/R) and is closely related to the pathogenesis of lipopolysaccharide (LPS) -induced septic ALI, and can aggravate further tissue and organ damage ( 73 , 105 ). Activation of NRF2 enhances resistance to lipid peroxidation induced lung injury by ferroptosis factors (GPX4, SlC7A11) in murine models of ALI, thereby protecting alveolar epithelial cells from ferroptosis ( 106 , 107 ).…”

Section: Ferroptosis In Pulmonary Diseasementioning

confidence: 99%

A deep insight into ferroptosis in lung disease: facts and perspectives

Zhang,

Xiang,

et al. 2024

Front. Oncol.

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In the last decade, ferroptosis has received much attention from the scientific research community. It differs from other modes of cell death at the morphological, biochemical, and genetic levels. Ferroptosis is mainly characterized by non-apoptotic iron-dependent cell death caused by iron-dependent lipid peroxide excess and is accompanied by abnormal iron metabolism and oxidative stress. In recent years, more and more studies have shown that ferroptosis is closely related to the occurrence and development of lung diseases. COPD, asthma, lung injury, lung fibrosis, lung cancer, lung infection and other respiratory diseases have become the third most common chronic diseases worldwide, bringing serious economic and psychological burden to people around the world. However, the exact mechanism by which ferroptosis is involved in the development and progression of lung diseases has not been fully revealed. In this manuscript, we describe the mechanism of ferroptosis, targeting of ferroptosis related signaling pathways and proteins, summarize the relationship between ferroptosis and respiratory diseases, and explore the intervention and targeted therapy of ferroptosis for respiratory diseases.

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Proanthocyanidins attenuates ferroptosis against influenza-induced acute lung injury in mice by reducing IFN-γ

Cited by 19 publications

References 39 publications

Comparison of disinfectants-induced gene expression profile: Potential adverse effects

Comparison of disinfectants-induced gene expression profile: Potential adverse effects

The elucidation of plasma lipidome profiles during severe influenza in a mouse model

A deep insight into ferroptosis in lung disease: facts and perspectives

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