Article
Cardiac & Cardiovascular Systems
Michael G. Paulus, Kathrin Renner, Alexander G. Nickel, Christoph Brochhausen, Katharina Limm, Elmar Zugner, Maria J. Baier, Steffen Pabel, Stefan Wallner, Christoph Birner, Andreas Luchner, Christoph Magnes, Peter J. Oefner, Klaus J. Stark, Stefan Wagner, Christoph Maack, Lars S. Maier, Katrin Streckfuss-Bomeke, Samuel Sossalla, Alexander Dietl
Summary: Tachycardiomyopathy is a reversible left ventricular dysfunction caused by rapid heart rate. This study used rabbit models and induced pluripotent stem cell-derived cardiomyocytes to investigate the mitochondrial dysfunctions in tachycardiomyopathy. The findings show depletion of tricarboxylic acid cycle intermediates, altered redox balance, and mitochondrial morphological changes. These patterns diverge from characteristic signs of other heart failure etiologies.
BASIC RESEARCH IN CARDIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Te Zhang, Jiannan Li, Guoqing Zhao
Summary: Mitochondria provide energy and regulate physiological and pathological processes, controlled by various quality mechanisms such as division, fusion, and mitophagy. Peripheral neuropathy has complex etiologies, but oxidative stress from mitochondrial damage is a common pathogenesis. Regulation and control of mitochondrial quality may offer potential treatments for peripheral neuropathy.
DNA AND CELL BIOLOGY
(2021)
Article
Multidisciplinary Sciences
Carola Mancini, Sabrina Gohlke, Francisco Garcia-Carrizo, Vyacheslav Zagoriy, Heike Stephanowitz, Tim J. Schulz
Summary: The decline in brown adipose tissue function during aging may contribute to metabolic disorders such as diabetes and obesity. Metabolites identified in the study were found to be associated with three biochemical processes - energy metabolism, nucleotide metabolism, and vitamin metabolism - which may be linked to dysfunction of brown adipocytes.
SCIENTIFIC REPORTS
(2021)
Review
Cell Biology
Junsheng Chen, Arthur Bassot, Fabrizio Giuliani, Thomas Simmen
Summary: ALS is a devastating neurodegenerative disease without cure, with a potential involvement of dysfunctional mitochondria-endoplasmic reticulum contacts (MERCs) leading to altered mitochondrial bioenergetics and oxidative stress. VAPB and VCP are key players in ALS pathogenesis, interacting with other mutant proteins and causing ER stress, inflammation, and motor neuron death. The dysfunction of MERCs in ALS triggers a cascade of pathological changes in the cell.
Article
Cell Biology
Elizabeth A. Thompson, Katherine Cascino, Alvaro A. Ordonez, Weiqiang Zhou, Ajay Vaghasia, Anne Hamacher-Brady, Nathan R. Brady, Im-Hong Sun, Rulin Wang, Avi Z. Rosenberg, Michael Delannoy, Richard Rothman, Katherine Fenstermacher, Lauren Sauer, Kathyrn Shaw-Saliba, Evan M. Bloch, Andrew D. Redd, Aaron A. R. Tobian, Maureen Horton, Kellie Smith, Andrew Pekosz, Franco R. D'Alessio, Srinivasan Yegnasubramanian, Hongkai Ji, Andrea L. Cox, Jonathan D. Powell
Summary: The study identifies a unique population of T cells expressing increased VDAC1 in severe and recovered COVID-19 patients, associated with mitochondrial dysfunction and apoptosis. Additionally, specific metabolic phenotypes of myeloid-derived suppressor cells in COVID-19 patients can distinguish between severe and mild disease. These findings offer insight into dysfunctional immune response in COVID-19 patients and potential for developing personalized therapeutic approaches.
Article
Biochemistry & Molecular Biology
Miguel A. Tejada, Ana I. Santos-Llamas, Lesley Escriva, Juan J. Tarin, Antonio Cano, Maria J. Fernandez-Ramirez, Paulina Nunez-Badinez, Bianca De Leo, Philippa T. K. Saunders, Victor Vidal, Florent Barthas, Katy Vincent, Patrick J. Sweeney, Rowland R. Sillito, James Douglas Armstrong, Jens Nagel, Raul Gomez
Summary: A new mouse model of endometriosis-associated pain, which evaluates non-evoked responses more relevant to the patient experience, was developed in this study. The model showed significant differences in pain responses and behavior measures between the endometriosis and control groups, providing a better preclinical platform for drug testing.
Article
Biochemistry & Molecular Biology
Uma D. Kabra, Charles Affourtit, Martin Jastroch
Summary: The development of obesity and type 2 diabetes is associated with impaired mitochondrial function and abnormal insulin secretion in pancreatic beta cells. Assessment of mitochondrial bioenergetic parameters with Seahorse extracellular flux technology can predict insulin secretion. High-fat feeding in mice led to decreased glucose sensitivity in islet respiration, highlighting the importance of mitochondrial function in regulating insulin secretion.
Article
Biochemistry & Molecular Biology
Arianna Barchiesi, Veronica Bazzani, Agata Jabczynska, Lukasz S. Borowski, Silke Oeljeklaus, Bettina Warscheid, Agnieszka Chacinska, Roman J. Szczesny, Carlo Vascotto
Summary: APE1 is a versatile protein involved in DNA repair, gene expression regulation, and RNA metabolism in mitochondria. Loss of APE1 leads to accumulation of damaged mitochondrial mRNA, impairing protein translation and mitochondrial respiration efficiency. The data demonstrate that APE1 plays a crucial role in maintaining mitochondrial well-being.
JOURNAL OF MOLECULAR BIOLOGY
(2021)
Article
Biology
Maria M. Cobo, Caroline Hartley, Deniz Gursul, Foteini Andritsou, Marianne van der Vaart, Gabriela Schmidt Mellado, Luke Baxter, Eugene P. Duff, Miranda Buckle, Ria Evans Fry, Gabrielle Green, Amy Hoskin, Richard Rogers, Eleri Adams, Fiona Moultrie, Rebeccah Slater
Summary: Despite the high burden of pain in hospitalised neonates, few analgesics have proven efficacy. Testing analgesics in neonates comes with challenges, both experimentally and ethically; however, EEG-derived measures of noxious-evoked brain activity can help assess efficacy. A new experimental paradigm accounting for individual differences in noxious-evoked baseline sensitivity was developed and tested across four studies, providing evidence of the efficacy of gentle brushing and paracetamol in neonates. This work represents an important step towards safe and cost-effective clinical trials of analgesics in neonates.
Article
Biochemistry & Molecular Biology
Noura Abdalla, Ester Tobias-Baraja, Alejandro Gonzalez, Gloria Garrabou, Gustavo Egea, Victoria Campuzano
Summary: Williams-Beuren syndrome (WBS) is a rare neurodevelopmental disorder characterized by a strong cardiovascular phenotype and a distinct neurocognitive profile. The cardiovascular features of WBS are primarily linked to the hemizygosity of the elastin (ELN) gene, but the phenotypic variability suggests the presence of additional modulators. Mitochondrial dysfunction and dynamics have been implicated as potential modulators, and a WBS complete deletion (CD) model exhibits similar mitochondrial phenotypes as observed in WBS patients.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Miguel Molina-Berenguer, Ferran Vila-Julia, Sandra Perez-Ramos, Maria Teresa Salcedo-Allende, Yolanda Camara, Javier Torres-Torronteras, Ramon Marti
Summary: Hepatoencephalopathy due to combined oxidative phosphorylation deficiency type 1 (COXPD1) is a mitochondrial translation disorder caused by mutations in GFM1. Mouse models with Gfm1 knock-in and knock-out mutations were generated to study COXPD1. The knock-in mice showed normal growth but had decreased mitochondrial EFG1 protein content, while the knock-out mice were embryonically lethal. The compound heterozygous mice had impaired mitochondrial translation and respiratory chain dysfunction, making them suitable for studying COXPD1.
Article
Cell Biology
Yu-Seon Han, Eui-Yeun Yi, Myeong-Eun Jegal, Yung-Jin Kim
Summary: Mitochondrial dysfunction can transform cancer cells into cancer stem-like cells, as shown by the generation of mitochondria dysfunctional (rho(0)) cells from the Hep3B hepatocellular carcinoma cell line. These rho(0) cells exhibited increased cancer stem-like properties, such as self-renewal, chemotherapy resistance, and angiogenesis. The data suggest that mitochondrial dysfunction plays a significant role in driving the transition of cancer cells towards a stem-like phenotype.
Review
Immunology
Maria-Jose Barrera, Sergio Aguilera, Isabel Castro, Patricia Carvajal, Daniela Jara, Claudio Molina, Sergio Gonzalez, Maria-Julieta Gonzalez
Summary: The dysfunction of mitochondria can disrupt cellular homeostasis and trigger inflammatory responses by releasing DAMPs, including cardiolipin, mtDNA, and formylated peptides. MERCs are crucial for maintaining calcium homeostasis and regulating inflammatory signaling, with alterations potentially contributing to autoimmune diseases. Understanding these mechanisms is essential for developing targeted therapies for inflammatory conditions.
AUTOIMMUNITY REVIEWS
(2021)
Review
Biochemistry & Molecular Biology
Alessandra Ghigo, Giulia Prono, Elisa Riccardi, Virginia De Rose
Summary: Cystic fibrosis (CF) is a genetic disorder caused by mutations in the CFTR gene, resulting in lung damage. Chronic airway inflammation plays a crucial role in the disease, and research on new anti-inflammatory drugs and treatments is crucial for improving the condition.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Cell Biology
Georg A. A. Petroianu, Lujain Aloum, Abdu Adem
Summary: Physiopathology and neurotransmission of pain are complex, and our ability to suppress chronic pain is limited. The number of clinically available medications is low and their success is modest. Pain Medicine practitioners face an ethical dichotomy, as they strive to adhere to the principle of primum non nocere while also aiming for successful pain relief. This article provides an overview of nociceptive pain, including nociceptive input, modulatory output, and local control. It also discusses the transition to neuropathic pain and the process of pain sensitization and chronification. The article then explores the sites and modes of action of clinically available drugs used in chronic pain treatment, with a focus on adjuvant medication.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2023)
