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Condition: Emphysema
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Total 35 results found since Jan 2013.
ROS induced the Rab26 promoter hypermethylation to promote cigarette smoking-induced airway epithelial inflammation of COPD through activation of MAPK signaling
In this study, we explore the role of Rab26 in CS exposure modulating the inflammatory response of airway epithelium and the novel mechanism of CS exposure regulation Rab26. These data showed that CS exposure and H2O2 (a type of ROS) suppressed the expression of Rab26 and increased the expression of DNMT3b in vivo and in vitro. GEO data analysis found the level of Rab26 was decreased in the lung tissue of COPD patients. CSE-induced ROS promoted DNA methylation of the Rab26 promoter and inhibited its promoter activity by elevating the DNMT3b level. Antioxidants N-Acetyl-l-cysteine (NAC), 5-Aza-2'-deoxycytidine (5-AZA) (DNA ...
Source: Free Radical Biology and Medicine - January 7, 2023 Category: Biology Authors: Bin-Feng He Yi-Xing Wu Wei-Ping Hu Jian-Lan Hua Yaoping Han Jing Zhang Source Type: research
Hydrogen sulfide alleviates particulate matter-induced emphysema and airway inflammation by suppressing ferroptosis
CONCLUSION: This research suggested that H2S alleviated PM-induced emphysema and airway inflammation via restoring redox balance and inhibiting ferroptosis through regulating Nrf2-PPAR-ferritinophagy signaling pathway.PMID:35490984 | DOI:10.1016/j.freeradbiomed.2022.04.014
Source: Free Radical Biology and Medicine - May 1, 2022 Category: Biology Authors: Ying Wang Sha Liao Zihan Pan Simin Jiang Jing Fan Siwang Yu Lixiang Xue Jianling Yang Shaohua Ma Tong Liu Jing Zhang Yahong Chen Source Type: research
Involvement of < em > NEAT1 < /em > /PINK1-mediated mitophagy in chronic obstructive pulmonary disease induced by cigarette smoke or PM < sub > 2.5 < /sub >
CONCLUSIONS: Our results suggest that CS and PM2.5 exposure induce mitochondrial dysfunction, and the NEAT1/PINK1 pathway plays a critical role in the occurrence and development of COPD by regulating mitophagy.PMID:35433942 | PMC:PMC9011272 | DOI:10.21037/atm-22-542
Source: Cancer Control - April 18, 2022 Category: Cancer & Oncology Authors: Qi Lin Chao-Feng Zhang Jin-Ling Guo Jian-Lin Su Zhen-Kun Guo Huang-Yuan Li Source Type: research
LL-37 and HMGB1 induce alveolar damage and reduce lung tissue regeneration via RAGE
Am J Physiol Lung Cell Mol Physiol. 2021 Aug 18. doi: 10.1152/ajplung.00138.2021. Online ahead of print.ABSTRACTThe receptor for advanced glycation end-products (RAGE) has been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). However, it is still unknown whether RAGE directly contributes to alveolar epithelial damage and abnormal repair responses. We hypothesize that RAGE activation not only induces lung tissue damage but also hampers alveolar epithelial repair responses. The effects of the RAGE ligands LL-37 and HMGB1 were examined on airway inflammation and alveolar tissue damage in wild...
Source: Am J Physiol Lung Ce... - August 18, 2021 Category: Respiratory Medicine Authors: Simon D Pouwels Laura Hesse Xinhui Wu Venkata Sita Rama Raju Allam Daan van Oldeniel Linsey J Bhiekharie Simon Phipps Brian G G Oliver Reinoud Gosens Maria Sukkar Irene H Heijink Source Type: research
