PM2.5-related cell death patterns

Wang, Yunxia; Zhong, Yingjie; Liao, Jiping; Wang, Guangfa

doi:10.7150/ijms.46421

Cited by 64 publications

(40 citation statements)

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“…Ferroptosis is a newly identified programed cell death that characterized by abnormal iron metabolism, lipid metabolism, oxidative stress, and glutathione (GSH) [11]. Increasing evidence has demonstrated that ferroptosis is correlated with various diseases, including cancer, cardiovascular diseases, and neurodegenerative diseases [12][13][14]. Besides, previous study has identified that ferroptosis participate in the progression of lung injury [15,16].…”

Section: Introductionmentioning

confidence: 99%

PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating Ferroptosis via TGF-β Signaling

et al. 2022

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Background. Lung fibrosis is a severe lung disorder featured by chronic nonspecific inflammation of the interstitial lung and deposition of collagen, leading to lung dysfunction. It has been identified that ferroptosis is involved in the progression of lung injury. Particulate matter (PM2.5) is reported to be correlated with the incidence of pulmonary fibrosis. However, mechanisms underlying ferroptosis in PM2.5-related lung fibrosis is unclear. In this study, we aimed to explore the effect of PM2.5 on ferroptosis in lung fibrosis and the related molecular mechanisms. Methods. PM2.5-treated mouse model and cell model were established. Fibrosis and tissue damage were measured by Masson’s trichrome staining and HE staining. Fibrosis biomarkers, such as α-SMA, collagen I, and collagen III, were examined by histological analysis. The ferroptosis phenotypes, including the levels of iron, Fe2+, MDA, and GSH, were measured by commercial kits. ROS generation was checked by DCFH-DA. The oxidative stress indicators, 3-nitro-L-tyrosine (3 ′ -NT), 4-HNE, and protein carbonyl, were checked by enzyme linked immunosorbent assay (ELISA). The thiobarbituric acid reactive substances (TBARS) and GSH/GSSG ratio were assessed by TBARS assay kit and GSH/GSSG assay kit, respectively. TGF-β signaling was detected by Western blotting. Results. PM2.5 induced the lung injury and fibrosis in the mice model, along with elevated expression of fibrosis markers. PM2.5 enhanced oxidative stress in the lung of the mice. The SOD2 expression was reduced, and NRF2 expression was enhanced in the mice by the treatment with PM2.5. PM2.5 triggered ferroptosis, manifested as suppressed expression of GPX4 and SLC7A11, decreased levels of iron, Fe2+, and MDA, and increased GSH level in mouse model and cell model. The TGF-β and Smad3 signaling was inhibited by PM2.5. ROS inhibitor NAC reversed PM2.5-regulated ROS and ferroptosis in primary mouse lung epithelial cells. Conclusions. Therefore, we concluded that PM2.5 exposure induced lung injury and fibrosis by inducing ferroptosis via TGF-β signaling.

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Section: Introductionmentioning

confidence: 99%

PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating Ferroptosis via TGF-β Signaling

et al. 2022

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“…Few new studies have focused on the function of particulate matter on men. Based on these research studies, autophagy, necrosis, apoptosis, pyroptosis, and ferroptosis are the most well-known side effects of PM 2.5 [51]. In our study, the average number of IHD was 27.92 cases.…”

Section: The Estimate Of the Ihd Incidence Related To Pm 25 Concentra...supporting

confidence: 49%

Assessment of Health Impacts of PM2.5 by AirQ+ Software in the City of Sanandaj, Iran (2018-2019)

Asgari

Khoshniyat

Karimi

et al. 2021

J Adv Environ Health Res

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Background: Particulate or particle mattes in term of air pollution are particles with a diameter of 2.5 μm or less (PM2.5). PM2.5 is a natural source of air pollution and has harmful effects on citizens in Sanandaj City, located in the west of Iran. Methods: In this study, the hourly data of concentration of PM2.5 were taken from the Kurdistan Environmental Protection Agency. During the study period (2018-2019), the 24-hour concentration of PM2.5 exceeded 339 times the average level. By AirQ+ software, the relationship between data and Relative Risk (RR), Baseline Incidence (BI), and Attributable Proportion (AP) were estimated. Then chronic obstructive pulmonary disease, lung cancer, ischemic heart disease, and brain stroke in the range of over 30 years were estimated. Results: The main target of this study was to survey the relationship between PM2.5 concentration and the death rate of citizens of this non-industrial city. The long-term health effect (more than 6 months) of PM2.5 caused 326 deaths on average (except for accidents and poisoning). Conclusion: Increase the concentration of PM2.5 is one factor that affects a high percentage of mortality rate.

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“…Clarifying its underlying mechanism is essential to determine effective prevention and treatment strategies. Based on previous reports, the mechanism of PM 2.5 -induced lung damage is complex, including oxidative stress, inflammation, apoptosis, necrosis, and autophagy, and all forms not only occur simultaneously but also overlap and crosstalk with one another. − Some studies have pointed out the anti-inflammatory and antioxidant effects of Ses. , Ses could reduce carrageenan-induced lung inflammation, and its anti-inflammatory mechanism was proven to be related with the inhibition of the NF-κB pathway, upregulation of A20 and reduction of polymorphonuclear neutrophil infiltration . In this research, we unveiled, for the first time, that Ses pretreatment could significantly ameliorate PM 2.5 -induced lung toxicity.…”

Section: Discussionmentioning

confidence: 68%

Sesamin Ameliorates Fine Particulate Matter (PM_2.5)-Induced Lung Injury via Suppression of Apoptosis and Autophagy in Rats

Ren

Zhu

et al. 2022

J. Agric. Food Chem.

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Lung damage can be caused by fine particulate matter (PM2.5). Thus, effective prevention strategies for PM2.5-induced lung injury are urgently required. Sesamin (Ses) is a natural polyphenolic compound that has attracted considerable attention of researchers because of its wide range of pharmacological activities. The present study aims to elucidate whether Ses pretreatment could alleviate PM2.5-induced lung damage and identify its possible mechanisms. Sprague–Dawley rats were orally dosed with 0.5% carboxymethylcellulose (CMC) and different concentrations of Ses once a day for 21 days. Then, the rats of the PM2.5 exposure group and Ses-treated group were exposed to PM2.5 by intratracheal instillation every 2 days for 1 week. Biomarkers associated with lung injury were detected in bronchoalveolar lavage fluid (BALF). Lung tissue was collected for histology, inflammation, oxidative stress, immunohistochemistry, and Western blot. Our results showed that PM2.5 exposure could cause pathological changes in lung tissue and increase levels of TP, AKP, and ALB in BALF. Meanwhile, exposure to PM2.5 can cause oxidative stress and inflammation in the lungs. In addition, Ses pretreatment could ameliorate histopathological injury, oxidative stress, and inflammation caused by PM2.5 exposure. It could also inhibit PM2.5-induced apoptosis and upregulation of autophagy-associated proteins. Collectively, our study indicated that Ses pretreatment could ameliorate PM2.5-induced lung damage via inhibiting apoptosis and autophagy in rats.

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PM2.5-related cell death patterns

Cited by 64 publications

References 50 publications

PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating Ferroptosis via TGF-β Signaling

PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating Ferroptosis via TGF-β Signaling

Assessment of Health Impacts of PM2.5 by AirQ+ Software in the City of Sanandaj, Iran (2018-2019)

Sesamin Ameliorates Fine Particulate Matter (PM_2.5)-Induced Lung Injury via Suppression of Apoptosis and Autophagy in Rats

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PM2.5-related cell death patterns

Cited by 64 publications

References 50 publications

PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating Ferroptosis via TGF-β Signaling

PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating Ferroptosis via TGF-β Signaling

Assessment of Health Impacts of PM2.5 by AirQ+ Software in the City of Sanandaj, Iran (2018-2019)

Sesamin Ameliorates Fine Particulate Matter (PM2.5)-Induced Lung Injury via Suppression of Apoptosis and Autophagy in Rats

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Sesamin Ameliorates Fine Particulate Matter (PM_2.5)-Induced Lung Injury via Suppression of Apoptosis and Autophagy in Rats