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Evidence for mitochondrial Lonp1 expression in the nucleus.
Sci Rep
June 2022
Department of Life Sciences, University of Modena and Reggio Emilia, Via Campi 287, 41125, Modena, Italy.
The coordinated communication between the mitochondria and nucleus is essential for cellular activities. Nonetheless, the pathways involved in this crosstalk are scarcely understood. The protease Lonp1 was previously believed to be exclusively located in the mitochondria, with an important role in mitochondrial morphology, mtDNA maintenance, and cellular metabolism, in both normal and neoplastic cells.
View Article and Find Full Text PDFAre Multiple Mitochondrial Related Signalling Pathways Involved in Carotid Body Oxygen Sensing?
Front Physiol
May 2022
School of Biomedical Sciences, Institute of Clinical Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Article Synopsis
- - The carotid body's type I cell mitochondria are sensitive to small decreases in oxygen levels, enabling it to act quickly as an oxygen sensor and trigger protective body reflexes before other cells' functions are impaired.
- - Several potential signaling mechanisms have been proposed to explain how decreased mitochondrial activity leads to type I cell depolarization, including the production of reactive oxygen species and changes in metabolic byproducts like lactate and ATP.
- - The review suggests that a single mechanism is unlikely, and instead multiple mitochondrial signaling pathways likely work together at varying oxygen levels during hypoxia, although it remains unclear how these pathways interact with other oxygen-sensing mechanisms.
Mitochondrial Dysfunction in Trauma-Related Coagulopathy: Is There Causality? Study Protocol for a Prospective Observational Study.
Eur Surg Res
June 2023
Department of Traumatology, University of Szeged, Szeged, Hungary.
Hemorrhage control often poses a great challenge for clinicians due to trauma-induced coagulopathy (TIC). The pathogenesis of TIC is not completely revealed; however, growing evidence attributes a central role to altered platelet biology. The activation of thrombocytes and subsequent clot formation are highly energetic processes being tied to mitochondrial activity, and the inhibition of the electron transport chain (ETC) impedes on thrombogenesis, suggesting the potential role of mitochondria in TIC.
View Article and Find Full Text PDFAnimal Models of Coenzyme Q Deficiency: Mechanistic and Translational Learnings.
Antioxidants (Basel)
October 2021
Departamento de Fisiología, Facultad de Medicina, Universidad de Granada, 18016 Granada, Spain.
Coenzyme Q (CoQ) is a vital lipophilic molecule that is endogenously synthesized in the mitochondria of each cell. The CoQ biosynthetic pathway is complex and not completely characterized, and it involves at least thirteen catalytic and regulatory proteins. Once it is synthesized, CoQ exerts a wide variety of mitochondrial and extramitochondrial functions thank to its redox capacity and its lipophilicity.
View Article and Find Full Text PDFMetabolomic Fingerprint of Mecp2-Deficient Mouse Cortex: Evidence for a Pronounced Multi-Facetted Metabolic Component in Rett Syndrome.
Cells
September 2021
Institut für Neuro- und Sinnesphysiologie, Zentrum Physiologie und Pathophysiologie, Universitätsmedizin Göttingen, Georg-August-Universität Göttingen, D-37130 Göttingen, Germany.
Using unsupervised metabolomics, we defined the complex metabolic conditions in the cortex of a mouse model of Rett syndrome (RTT). RTT, which represents a cause of mental and cognitive disabilities in females, results in profound cognitive impairment with autistic features, motor disabilities, seizures, gastrointestinal problems, and cardiorespiratory irregularities. Typical RTT originates from mutations in the X-chromosomal methyl-CpG-binding-protein-2 () gene, which encodes a transcriptional modulator.
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