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Biomedicines
Special Issues
Mitochondria in Human Health and Diseases
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Mitochondria in Human Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 4607

Special Issue Editor

Dr. Yong Zhao

E-Mail Website
Guest Editor
Throne Biotechnologies, Paramus, NJ 07652, USA
Interests: cord blood stem cell; type 1 diabetes; autoimmune disease; Stem Cell Educator therapy; immune modulation; mitochondria; exosome

Special Issue Information

Dear Colleagues,

Mitochondria, an energy center integrating with other organelles, contribute to a variety of cellular activities and stress responses through their dynamic properties such as fusion, fission and mitophagy, leading to the maintenance of cellular homeostasis. Recent advances in mitochondrial biology demonstrate that mitochondria not only act as organelles of “a cellular power plant” for ATP production to energize cellular/molecular activities of daily life, but also circulate in human peripheral blood and function as novel mediators involved in the crosstalk among different cells, tissues, and organs in physiological and pathological conditions. Increasing evidence demonstrates that mitochondria dominate the proliferation and differentiation of stem cells. Notably, mitochondria can penetrate the nuclear membrane, leading to cellular reprogramming and the generation of autologous multipotent stem cells. Interestingly, the purified mitochondria display immune modulation on the activated human T cells and the central/effector memory T cells. Therefore, targeting the mitochondrial system may facilitate the clarification of the pathogenesis of different diseases and hold tremendous therapeutic potentials to treat the inflammation-associated diseases, diabetes, autoimmune diseases, cancer, neurodegenerative diseases, and others. This Special Issue focuses on recent progress in basic research and clinical studies of mitochondria to facilitate their translational potential in clinics. Researchers and clinicians are encouraged to submit insightful reviews and research papers on the topic of mitochondria.

Dr. Yong Zhao
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly 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

  • mitochondrial biology
  • stem cells
  • cell growth and differentiation
  • immune cells
  • inflammation
  • autoimmunity
  • diabetes
  • neurodegenerative diseases
  • aging
  • clinical trials

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Published Papers (3 papers)

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Research

17 pages, 5579 KiB  
Article
Effects of Anesthesia with Pentobarbital/Ketamine on Mitochondrial Permeability Transition Pore Opening and Ischemic Brain Damage
by Evelina Rekuviene, Laima Ivanoviene, Vilmante Borutaite and Ramune Morkuniene
Biomedicines 2024, 12(10), 2342; https://doi.org/10.3390/biomedicines12102342 - 15 Oct 2024
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Abstract
Background and Objective: The alteration of mitochondrial functions, especially the opening of the mitochondrial permeability transition pore (mPTP), has been proposed as a key mechanism in the development of lesions in cerebral ischemia, wherefore it is considered as an important target for drugs [...] Read more.
Background and Objective: The alteration of mitochondrial functions, especially the opening of the mitochondrial permeability transition pore (mPTP), has been proposed as a key mechanism in the development of lesions in cerebral ischemia, wherefore it is considered as an important target for drugs against ischemic injury. In this study, we aimed to investigate the effects of mitochondrial complex I inhibitors as possible regulators of mPTP using an in vitro brain ischemia model of the pentobarbital/ketamine (PBK)-anesthetized rats. Results: We found that PBK anesthesia itself delayed Ca2+-induced mPTP opening and partially recovered the respiratory functions of mitochondria, isolated from rat brain cortex and cerebellum. In addition, PBK reduced cell death in rat brain slices of cerebral cortex and cerebellum. PBK inhibited the adenosine diphosphate (ADP)-stimulated respiration of isolated cortical and cerebellar mitochondria respiring with complex I-dependent substrates pyruvate and malate. Moreover, pentobarbital alone directly increased the resistance of isolated cortex mitochondria to Ca2+-induced activation of mPTP and inhibited complex I-dependent respiration and mitochondrial complex I activity. In contrast, ketamine had no direct effect on functions of isolated normal cortex and cerebellum mitochondria. Conclusions: Altogether, this suggests that modulation of mitochondrial complex I activity by pentobarbital during PBK anesthesia may increase the resistance of mitochondria to mPTP opening, which is considered the key event in brain cell necrosis during ischemia. Full article
(This article belongs to the Special Issue Mitochondria in Human Health and Diseases)
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11 pages, 1350 KiB  
Article
The Interplay between Mitochondrial Metabolism and Nasal Mucociliary Function as a Surrogate Method to Diagnose Thyroid Dysfunction: Insights from a Population-Based Study
by Mohammad Farhadi, Hadi Ghanbari, Ali Salehi, Sumel Ashique and Farzad Taghizadeh-Hesary
Biomedicines 2024, 12(8), 1897; https://doi.org/10.3390/biomedicines12081897 - 20 Aug 2024
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Abstract
Aim and Background. This study aims to explore alternative diagnostic methods to assess thyroid function in patients unable to undergo blood tests for thyroid-stimulating hormones (TSH) and thyroxine (T4), such as individuals with trypanophobia, severe medical conditions, or coagulopathy. Considering the impact [...] Read more.
Aim and Background. This study aims to explore alternative diagnostic methods to assess thyroid function in patients unable to undergo blood tests for thyroid-stimulating hormones (TSH) and thyroxine (T4), such as individuals with trypanophobia, severe medical conditions, or coagulopathy. Considering the impact of thyroid dysfunction on mitochondrial metabolism and the essential role of proper mitochondrial function in ciliary motility, we postulate that assessing nasal ciliary function could serve as a surrogate diagnostic approach for thyroid dysfunction. Methods. This cross-sectional study was performed on individuals with no history of thyroid diseases. The primary endpoint was the diagnostic value of the nasal mucociliary (NMC) test using Iranica Picris (Asteraceae) aqueous extract in differentiating hypo- or hyperthyroidism cases from euthyroid cases. Results. 232 individuals were recruited (71% females, 86% euthyroid). Receiver operating characteristic (ROC) analysis showed a good diagnostic value for the NMC test in differentiating overt hypothyroidism (area under the ROC curve [AUROC] = 0.82, p = 0.004) and its fair value in diagnosing subclinical hyperthyroidism (AUROC = 0.78, p = 0.01) from the euthyroid condition. The NMC test had a significant positive correlation with TSH (r = 0.47, p < 0.001) and a significant negative correlation with T4 (r = −0.32, p < 0.001). The NMC rate was significantly different in distinct thyroid function groups (p < 0.001). Compared with euthyroid cases, the post-hoc analysis showed that the NMC test is significantly higher in overt hypothyroidism (15.06 vs. 21.07 min, p = 0.003) and significantly lower in subclinical hyperthyroidism (15.05 vs. 10.9 min, p = 0.02). Conclusions. The Iranica Picris-based NMC test might serve as a diagnostic method to distinguish overt hypothyroidism and subclinical hyperthyroidism. Full article
(This article belongs to the Special Issue Mitochondria in Human Health and Diseases)
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14 pages, 1639 KiB  
Article
Male and Female Mitochondria Respond Differently after Exercising in Acute Hypoxia
by Ylenia Lai, Francesco Loy, Michela Isola, Roberta Noli, Andrea Rinaldi, Carla Lobina, Romina Vargiu, Flaminia Cesare Marincola and Raffaella Isola
Biomedicines 2023, 11(12), 3149; https://doi.org/10.3390/biomedicines11123149 - 26 Nov 2023
Viewed by 1491
Abstract
The use of hypoxic devices among athletes who train in normobaric hypoxia has become increasingly popular; however, the acute effects on heart and brain metabolism are not yet fully understood. This study aimed to investigate the mitochondrial bioenergetics in trained male and female [...] Read more.
The use of hypoxic devices among athletes who train in normobaric hypoxia has become increasingly popular; however, the acute effects on heart and brain metabolism are not yet fully understood. This study aimed to investigate the mitochondrial bioenergetics in trained male and female Wistar rats after acute hypoxia training. The experimental plan included exercising for 30 min on a treadmill in a Plexiglas cage connected to a hypoxic generator set at 12.5% O2 or in normoxia. After the exercise, the rats were sacrificed, and their mitochondria were isolated from their brains and hearts. The bioenergetics for each complex of the electron transport chain was tested using a Clark-type electrode. The results showed that following hypoxia training, females experienced impaired oxidative phosphorylation through complex II in heart subsarcolemmal mitochondria, while males had an altered ADP/O in heart interfibrillar mitochondria, without any change in oxidative capacity. No differences from controls were evident in the brain, but an increased electron transport system efficiency was observed with complex I and IV substrates in males. Therefore, the study’s findings suggest that hypoxia training affects the heart mitochondria of females more than males. This raises a cautionary flag for female athletes who use hypoxic devices. Full article
(This article belongs to the Special Issue Mitochondria in Human Health and Diseases)
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