Role of Mitochondrial DNA in Inflammatory Airway Diseases

Snyder, Ryan J.; Kleeberger, Steven R.

doi:10.1002/cphy.c200010

Cited by 3 publications

(2 citation statements)

References 167 publications

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“…There has been an extensive research initially for inhaled insulin for patients with asthma and chronic obstructive pulmonary disease (COPD) [3]. The mucus, airway clearance mechanisms and local genes/transporters play a crucial role in the local absorption of an inhaled drug [23]. The viscosity of the mucus does not let the drug to be released to the airway surface [1].…”

Section: Discussionmentioning

confidence: 99%

Modification Tadalafil and Macitentan tablets to aerosol

Petridis¹,

Sardeli²,

Kosmıdis³

et al. 2022

Front. Biosci. (Landmark Ed)

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Introduction: Aerosolised drugs have been approved for several diseases such as cystic fibrosis and diabetes. Moreover; there are already drugs for pulmonary hypertension in aerosol form already on the market. Materials and methods: Two drugs for pulmonary hypertension (Tadalafil and Macitentan) were milled and transformed from tablets to powder. Three different jet-nebulizers with seven different residual cups were combined. Moreover, we used 3 different ultrasound nebulizers with two different release methods. Results: The drug and residual cup designs produce alone or jointly different MMAD diameters. The three large (10 mls) residual cups with the jet-nebulisers produced the smallest aerosol droplets. Both ultrasound nebulisers are capable of producing optimal size aerosol droplets ≤5 µm mmad. Conclusions: These two drugs can be easily administered as aerosol and an vivo clinical study will prove the safety for the airways.

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Section: Discussionmentioning

confidence: 99%

Modification Tadalafil and Macitentan tablets to aerosol

Petridis¹,

Sardeli²,

Kosmıdis³

et al. 2022

Front. Biosci. (Landmark Ed)

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“…Excessive ROS causes mitochondrial lysis and disrupts the dynamic homeostasis of mitochondria. Mitochondrial dynamics are related to ROS [46,47]. Drp1 is an important mitochondrial ssion-related factor and a key regulator of mitochondrial ssion [48].…”

Section: Discussionmentioning

confidence: 99%

Lipoxin A4 Ameliorates Lung Development in Neonatal Rats with Hyperoxia-induced Bronchopulmonary Dysplasia by Reducing Mitochondrial Fission

Yu,

Liang,

Zhu

et al. 2021

Preprint

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Bronchopulmonary dysplasia (BPD) is a common chronic pulmonary disease in premature infants. Hyper oxygen exposure and mechanical ventilation are common causes. The pulmonary pathological changes of BPD were mainly micro alveolar simplification and pulmonary vascular development disorder. Lipoxin A4(LXA4) is an important endogenous lipid and anti-inflammatory mediator that promotes the regression of inflammation and is referred to as the brake signal of inflammatory response. The purpose of this study was to evaluate the intervention of LXA4 on pulmonary inflammation and oxidative stress in neonates with hyperoxia lung injury and to explore the mechanism of Drp1 and NLRP3 inflammasome. A BPD model was established 7 days after neonatal rats were exposed to 85% oxygen. Rats were divided in four groups: control, hyperoxia, hyperoxia + LXA4 and hyperoxia+LXA4+Mdivi-1. Lung injury was evaluated via histological examination; lung development was assessed using morphometric analyses. Pulmonary micro vessels were tested by vWF-positive staining and Evans Blue. Expression of Drp1, NF-κB, and NLRP3 was analyzed via western blot or immunohistochemistry. Dihydroethidium (DHE) levels was examined to determine oxidative stress in vitro. We found that LXA4 significantly reduced lung injury of rats, simplified alveoli, and promoted weight gain. In addition, we found that LXA4 can reduce the protein expression of pDrp1, pNF-κB and NLRP3. Therefore, we concluded that LXA4 intervention can reduce the inflammatory response in the lungs and reduce the degree of lung injury, and through the role of NLRP3 inflammatory chrome in the hypertoxic rat BPD model.

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Variability of Mitochondrial DNA Heteroplasmy: Association with Asymptomatic Carotid Atherosclerosis

Sazonova,

Kirichenko,

Ryzhkova

et al. 2024

Biomedicines

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Background and Objectives: Atherosclerosis is one of the main reasons for cardiovascular disease development. This study aimed to analyze the association of mtDNA mutations and atherosclerotic plaques in carotid arteries of patients with atherosclerosis and conditionally healthy study participants from the Novosibirsk region. Methods: PCR fragments of DNA containing the regions of 10 investigated mtDNA mutations were pyrosequenced. The heteroplasmy levels of mtDNA mutations were analyzed using a quantitative method based on pyrosequencing technology developed by M. A. Sazonova and colleagues. Results: In the analysis of samples of patients with atherosclerotic plaques of the carotid arteries and conditionally healthy study participants from the Novosibirsk region, four proatherogenic mutations in the mitochondrial genome (m.5178C>A, m.652delG, m.12315G>A and m.3256C>T) and three antiatherogenic mutations in mtDNA (m.13513G>A, m.652insG, and m.14846G>A) were detected. A west–east gradient was found in the distribution of the mtDNA mutations m.5178C>A, m.3256C>T, m.652insG, and m.13513G>A. Conclusions: Therefore, four proatherogenic mutations in the mitochondrial genome (m.5178C>A, m.652delG, m.12315G>A, and m.3256C>T) and three antiatherogenic mutations in mtDNA (m.13513G>A, m.652insG, and m.14846G>A) were detected in patients with atherosclerotic plaques in their carotid arteries from the Novosibirsk region.

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Role of Mitochondrial DNA in Inflammatory Airway Diseases

Cited by 3 publications

References 167 publications

Modification Tadalafil and Macitentan tablets to aerosol

Modification Tadalafil and Macitentan tablets to aerosol

Lipoxin A4 Ameliorates Lung Development in Neonatal Rats with Hyperoxia-induced Bronchopulmonary Dysplasia by Reducing Mitochondrial Fission

Variability of Mitochondrial DNA Heteroplasmy: Association with Asymptomatic Carotid Atherosclerosis

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