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Mitochondria in Pulmonary Disease: From Molecular Mechanism to Medicine
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Mitochondria in Pulmonary Disease: From Molecular Mechanism to Medicine

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Pulmonology".

Deadline for manuscript submissions: closed (25 June 2022) | Viewed by 5068

Special Issue Editors

Prof. Dr. Natascha Sommer

E-Mail Website
Guest Editor
Excellence Cluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Justus-Liebig-University, 35392 Giessen, Germany
Interests: lung function and hemodynamic measurements; histology; mitochondrial function; targeted antioxidants; hypoxia; acute respiratory distress syndrome; pulmonary hypertension
Special Issues, Collections and Topics in MDPI journals
Dr. Oleg Pak

E-Mail Website
Co-Guest Editor
Excellence Cluster Cardio-Pulmonary Institute (CPI), University of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL), Justus-Liebig-University of Giessen, 35392 Giessen, Germany
Interests: mitochondria; oxygen sensing; pulmonary emphysema; pulmonary hypertension; cytochrome c oxidase

Special Issue Information

Dear Colleagues,

In lung diseases, mitochondria have become the focus of attention owing to their role as a central hub for the integration and transformation of cellular signals, thereby regulating, e.g., inflammation, proliferation, apoptosis, and contraction. In addition, mitochondria act as primary sensors for hypoxia and allow for the availability of substrates that are utilized for ATP production. Mitochondrial release of reactive oxygen species, interference with intracellular calcium homeostasis, and modulation of metabolic intermediates play an important role in the development of various pathologies, e.g., pulmonary hypertension, emphysema, pulmonary fibrosis, and lung cancer, but also in physiological signaling processes such as hypoxia-dependent signaling and the activation of immune cells. Although a large number of animal models have shown the effectiveness of targeting mitochondria for the treatment of various pulmonary diseases, currently, translation into clinic is very limited.

The aim of this Special Issue is to present clinical and experimental scientific reports that provide a deeper understanding of the physiological and pathological mitochondrial signal processes that allow for the development of new treatment strategies and the implementation of experimental concepts in clinical practice.

Dr. Natascha Sommer
Guest Editors
Dr. Oleg Pak
Co-Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondria
  • lung disease
  • reactive oxygen species
  • COPD
  • pulmonary hypertension
  • pulmonary fibrosis
  • pulmonary inflammation
  • lung cancer
  • hypoxia
  • metabolism

Published Papers (3 papers)

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Research

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13 pages, 1818 KiB  
Article
Chronic Lung Allograft Dysfunction Is Associated with Increased Levels of Cell-Free Mitochondrial DNA in Bronchoalveolar Lavage Fluid of Lung Transplant Recipients
by Emmanuel Schneck, Ingolf Askevold, Ramona Rath, Andreas Hecker, Martin Reichert, Stefan Guth, Christian Koch, Michael Sander, Werner Seeger, Konstantin Mayer, Winfried Padberg, Natascha Sommer, Stefan Kuhnert and Matthias Hecker
J. Clin. Med. 2022, 11(14), 4142; https://doi.org/10.3390/jcm11144142 - 16 Jul 2022
Cited by 1 | Viewed by 1595
Abstract
Chronic Lung Allograft Dysfunction (CLAD) is a life-threatening complication that limits the long-term survival of lung transplantation patients. Early diagnosis remains the basis of efficient management of CLAD, making the need for distinctive biomarkers critical. This explorative study aimed to investigate the predictive [...] Read more.
Chronic Lung Allograft Dysfunction (CLAD) is a life-threatening complication that limits the long-term survival of lung transplantation patients. Early diagnosis remains the basis of efficient management of CLAD, making the need for distinctive biomarkers critical. This explorative study aimed to investigate the predictive power of mitochondrial DNA (mtDNA) derived from bronchoalveolar lavages (BAL) to detect CLAD. The study included 106 lung transplant recipients and analyzed 286 BAL samples for cell count, cell differentiation, and inflammatory and mitochondrial biomarkers, including mtDNA. A receiver operating curve analysis of mtDNA levels was used to assess its ability to detect CLAD. The results revealed a discriminatory pro-inflammatory cytokine profile in the BAL fluid of CLAD patients. The concentration of mtDNA increased in step with each CLAD stage, reaching its highest concentration in stage 4, and correlated significantly with decreasing FEV1. The receiver operating curve analysis of mtDNA in BAL revealed a moderate prediction of CLAD when all stages were grouped together (AUROC 0.75, p-value < 0.0001). This study has found the concentration mtDNA in BAL to be a potential predictor for the early detection of CLAD and the differentiation of different CLAD stages, independent of the underlying pathology. Full article
(This article belongs to the Special Issue Mitochondria in Pulmonary Disease: From Molecular Mechanism to Medicine)
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12 pages, 1128 KiB  
Article
Minimized Extracorporeal Circulation Is Associated with Reduced Plasma Levels of Free-Circulating Mitochondrial DNA Compared to Conventional Cardiopulmonary Bypass: A Secondary Analysis of an Exploratory, Prospective, Interventional Study
by Thomas Zajonz, Christian Koch, Jan Schwiddessen, Melanie Markmann, Matthias Hecker, Fabian Edinger, Götz Schmidt, Andreas Boening, Michael Sander and Emmanuel Schneck
J. Clin. Med. 2022, 11(11), 2994; https://doi.org/10.3390/jcm11112994 - 25 May 2022
Cited by 2 | Viewed by 1707
Abstract
The use of minimized extracorporeal circulation (MiECC) during cardiac surgery is associated with a reduced inflammatory reaction compared to conventional cardiopulmonary bypass (cCPB). Since it is unknown if MiECC also reduces the amount of free-circulating mitochondrial DNA (mtDNA), this study aims to compare [...] Read more.
The use of minimized extracorporeal circulation (MiECC) during cardiac surgery is associated with a reduced inflammatory reaction compared to conventional cardiopulmonary bypass (cCPB). Since it is unknown if MiECC also reduces the amount of free-circulating mitochondrial DNA (mtDNA), this study aims to compare MiECC-induced mtDNA release to that of cCPB as well as to identify potential relations between the plasma levels of mtDNA and an adverse outcome. Overall, 45 patients undergoing cardiac surgery with either cCPB or MiECC were included in the study. MtDNA encoding for NADH dehydrogenase 1 was quantified with quantitative polymerase chain reaction. The plasma amount of mtDNA was significantly lower in patients undergoing cardiac surgery with MiECC compared to cCPB (MiECC: 161.8 (65.5–501.9); cCPB 190.8 (82–705.7); p < 0.001). Plasma levels of mtDNA showed comparable kinetics independently of the study group and peaked during CPB (MiECC preoperative: 68.2 (26.5–104.9); MiECC 60 min after start of CPB: 536.5 (215.7–919.6); cCPB preoperative: 152.5 (80.9–207.6); cCPB 60 min after start of CPB: 1818.0 (844.2–3932.2); all p < 0.001). Patients offering an mtDNA blood concentration of >650 copies/µL after the commencement of CPB had a 5-fold higher risk for postoperative atrial fibrillation independently of the type of cardiopulmonary bypass. An amount of mtDNA being higher than 650 copies/µL showed moderate predictive power (AUROC 0.71 (0.53–071)) for the identification of postoperative atrial fibrillation. In conclusion, plasma levels of mtDNA were lower in patients undergoing cardiac surgery with MiECC compared to cCPB. The amount of mtDNA at the beginning of the CPB was associated with postoperative atrial fibrillation independent of the type of cardiopulmonary bypass. Full article
(This article belongs to the Special Issue Mitochondria in Pulmonary Disease: From Molecular Mechanism to Medicine)
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Review

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16 pages, 1154 KiB  
Review
Mitochondrial Regulation of the Hypoxia-Inducible Factor in the Development of Pulmonary Hypertension
by Esraa M. Zeidan, Mohammad Akbar Hossain, Mahmoud El-Daly, Mohammed A. S. Abourehab, Mohamed M. A. Khalifa and Ashraf Taye
J. Clin. Med. 2022, 11(17), 5219; https://doi.org/10.3390/jcm11175219 - 03 Sep 2022
Cited by 3 | Viewed by 2624
Abstract
Pulmonary hypertension (PH) is a severe progressive lung disorder characterized by pulmonary vasoconstriction and vascular remodeling, culminating in right-sided heart failure and increased mortality. Data from animal models and human subjects demonstrated that hypoxia-inducible factor (HIF)-related signaling is essential in the progression of [...] Read more.
Pulmonary hypertension (PH) is a severe progressive lung disorder characterized by pulmonary vasoconstriction and vascular remodeling, culminating in right-sided heart failure and increased mortality. Data from animal models and human subjects demonstrated that hypoxia-inducible factor (HIF)-related signaling is essential in the progression of PH. This review summarizes the regulatory pathways and mechanisms of HIF-mediated signaling, emphasizing the role of mitochondria in HIF regulation and PH pathogenesis. We also try to determine the potential to therapeutically target the components of the HIF system for the management of PH. Full article
(This article belongs to the Special Issue Mitochondria in Pulmonary Disease: From Molecular Mechanism to Medicine)
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