Ferroptosis is involved in PM2.5-induced acute nasal epithelial injury via AMPK-mediated autophagy

Gu, Wenjing; Hou, Tianhua; Zhou, Hongwei; Zhu, Laiyu; Zhu, Wei; Wang, Yusheng

doi:10.1016/j.intimp.2022.109658

Cited by 15 publications

(6 citation statements)

References 32 publications

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“…Interestingly, the levels of nuclear factor erythroid 2-related factor 2 (Nrf2), a key regulator of cellular oxidant resistance, were increased in the nucleus and decreased in the cytoplasm after PM2.5 treatment, suggesting that the nuclear translocation of Nrf2 was inhibited [35,37]. Analogous to these findings, Hong et al demonstrated that GSH-Px was downregulated in the nasal mucosa of rats exposed to PM2.5 and Gu et al demonstrated that PM2.5 exposure decreased GSH and increased MDA levels in human nasal epithelial cells [36,38].…”

Section: Disruption Of Epithelial Cell Metabolismmentioning

confidence: 92%

“…It was found that PM2.5 exposure induced phosphorylation of AMPKα and reduced expression of ferroptosis-related proteins such as GPx4, xCT, FTH1, and FTL. These changes led to autophagy and ferroptosis induction in nasal epithelial cells [38].…”

Section: Disruption Of Epithelial Cell Metabolismmentioning

confidence: 99%

“…Changes in the composition such as acidification of the mucus may cause impaired host defenses and increase the presence of airway bacteria [55]. Moreover, Gu et al showed that PM2.5 caused increased mucus secretion in the nasal mucosa of mice [38]. The effects of PM2.5 on nasal epithelial cells are summarized in Figure 1.…”

Section: Mucociliary Clearance Dysfunctionmentioning

confidence: 99%

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The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases

Zaręba,

Piszczatowska,

Dżaman

et al. 2024

JPM

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PM2.5 is one of the most harmful components of airborne pollution and includes particles with diameters of less than 2.5 μm. Almost 90% of the world’s population lives in areas with poor air quality exceeding the norms established by the WHO. PM2.5 exposure affects various organs and systems of the human body including the upper respiratory tract which is one of the most prone to its adverse effects. PM2.5 can disrupt nasal epithelial cell metabolism, decrease the integrity of the epithelial barrier, affect mucociliary clearance, and alter the inflammatory process in the nasal mucosa. Those effects may increase the chance of developing upper respiratory tract diseases in areas with high PM2.5 pollution. PM2.5’s contribution to allergic rhinitis (AR) and rhinosinusitis was recently thoroughly investigated. Numerous studies demonstrated various mechanisms that occur when subjects with AR or rhinosinusitis are exposed to PM2.5. Various immunological changes and alterations in the nasal and sinonasal epithelia were reported. These changes may contribute to the observations that exposure to higher PM2.5 concentrations may increase AR and rhinosinusitis symptoms in patients and the number of clinical visits. Thus, studying novel strategies against PM2.5 has recently become the focus of researchers’ attention. In this review, we summarize the current knowledge on the effects of PM2.5 on healthy upper respiratory tract mucosa and PM2.5’s contribution to AR and rhinosinusitis. Finally, we summarize the current advances in developing strategies against PM2.5 particles’ effects on the upper respiratory tract.

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Section: Disruption Of Epithelial Cell Metabolismmentioning

confidence: 92%

Section: Disruption Of Epithelial Cell Metabolismmentioning

confidence: 99%

Section: Mucociliary Clearance Dysfunctionmentioning

confidence: 99%

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The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases

Zaręba,

Piszczatowska,

Dżaman

et al. 2024

JPM

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“…Ferroptosis is an iron ion–dependent form of cell death triggered by the toxic overaccumulation of lipid peroxides on cell membranes, and its pathogenesis and resulting morphology differ from those of other forms of cell death such as apoptosis and autophagy (Dixon et al 2012 ). Several authors have confirmed that PM2.5 can cause damage to various systems, with ferroptosis being observed in the circulatory, respiratory, and digestive systems (Gu et al 2023 ; Guohua et al 2021 ; Hu et al 2023 ; Park et al 2023 ; Wang and Tang 2019 ). The mechanisms associated with ferroptosis are widely recognized as iron overload, lipid peroxidation, and the dysregulation of System Xc − activity; reproductive system damage is also strongly associated with ferroptosis (Li et al 2018 ).…”

Section: Introductionmentioning

confidence: 93%

PM 2.5 juvenile exposure–induced spermatogenesis dysfunction by triggering testes ferroptosis and antioxidative vitamins intervention in adult male rats

Liu,

Ai,

Xiao

et al. 2023

Environ Sci Pollut Res

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PM2.5 derived from automobile exhaust can cause reproductive impairment in adult males, but the toxic effects of PM2.5 exposure on reproductive function in juvenile male rats and its relationship with ferroptosis have not been reported. In this paper, 30-day-old juvenile male Sprague-Dawley (SD) rats were divided into four groups (blank control, vitamin control, PM2.5, and PM2.5+Vitamin). The blank control group was fed normally, and the vitamin control group was given intragastric administration of vitamins in addition to normal feeding. PM2.5 was administered via tracheal intubation. When the rats were treated for 4 weeks until reaching the period of sexual maturity. A mating test was performed first, and then their testicular and epididymal tissues were studied. Compared with control rats, juvenile male rats exposed to PM2.5 showed a decreased sperm count and fertility rate, redox imbalance, damaged mitochondria, a metabolic disorder of intracellular iron ions, and a significant rise in ferroptosis during the period of sexual maturity. After antioxidative vitamins intervention, the redox imbalance, metabolic disorder of intracellular iron ions, and ferroptosis were all alleviated, leading to the following conclusions: after being exposed to PM2.5 from automobile exhaust, male juvenile rats during the period of sexual maturity have significantly decreased reproductive function. The reproductive toxicity of PM2.5 is closely related to oxidative stress and ferroptosis. In addition, ferroptosis decreases and reproductive function is recovered to some degree after antioxidative vitamins intervention. Graphical abstract

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“…FTH1, on the other hand, plays a role in the regulation of ferritinophagy, helping cells to release or store iron ions as needed. These processes are essential for maintaining intracellular iron homeostasis (Gu et al, 2023).…”

Section: Ferritinophagy and Hccmentioning

confidence: 99%

Natural products targeting macroautophagy signaling in hepatocellular carcinoma therapy: Recent evidence and perspectives

Chen,

Tan,

Zhang

et al. 2024

Phytotherapy Research

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Hepatocellular carcinoma (HCC), presently the second leading cause of global cancer‐related mortality, continues to pose significant challenges in the realm of medical oncology, impacting both clinical drug selection and mechanistic research. Recent investigations have unveiled autophagy‐related signaling as a promising avenue for HCC treatment. A growing body of research has highlighted the pivotal role of autophagy‐modulating natural products in inhibiting HCC progression. In this context, we provide a concise overview of the fundamental autophagy mechanism and delineate the involvement of autophagic signaling pathways in HCC development. Additionally, we review pertinent studies demonstrating how natural products regulate autophagy to mitigate HCC. Our findings indicate that natural products exhibit cytotoxic effects through the induction of excessive autophagy, simultaneously impeding HCC cell proliferation by autophagy inhibition, thereby depriving HCC cells of essential energy. These effects have been associated with various signaling pathways, including PI3K/AKT, MAPK, AMPK, Wnt/β‐catenin, Beclin‐1, and ferroautophagy. These results underscore the considerable therapeutic potential of natural products in HCC treatment. However, it is important to note that the present study did not establish definitive thresholds for autophagy induction or inhibition by natural products. Further research in this domain is imperative to gain comprehensive insights into the dual role of autophagy, equipping us with a better understanding of this double‐edged sword in HCC management.

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Ferroptosis is involved in PM2.5-induced acute nasal epithelial injury via AMPK-mediated autophagy

Cited by 15 publications

References 32 publications

The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases

The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases

PM 2.5 juvenile exposure–induced spermatogenesis dysfunction by triggering testes ferroptosis and antioxidative vitamins intervention in adult male rats

Natural products targeting macroautophagy signaling in hepatocellular carcinoma therapy: Recent evidence and perspectives

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