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243 results for “Mitochondrial Dysfunction”
Dataset related to: Shiga Toxin 2 Triggers C3a-Dependent Glomerular and Tubular Injury through Mitochondrial Dysfunction in Hemolytic Uremic Syndrome
<p>The files contain all the dataset included in the manuscript, divided by figure in each tab.</p> <p> </p> <p><strong>Abstract</strong></p> <p>Shiga toxin (Stx)-producing <em>Escherichia coli</em> is the predominant offending agent of post-diarrheal hemolytic uremic syndrome (HUS), a rare disorder of microvascular thrombosis and acute kidney injury possibly leading to long-term renal sequelae. We previously showed that C3a has a critical role in the development of glomerular damage in experimental HUS. Based on the evidence that activation of C3a/C3a receptor (C3aR) signaling induces mitochondrial dysregulation and cell injury, here we investigated whether C3a caused podocyte and tubular injury through induction of mitochondrial dysfunction in a mouse model of HUS. Mice coinjected with Stx2/LPS exhibited glomerular podocyte and tubular C3 deposits and C3aR overexpression associated with cell damage, which were limited by C3aR antagonist treatment. C3a promoted renal injury by affecting mitochondrial wellness as demonstrated by data showing that C3aR blockade reduced mitochondrial ultrastructural abnormalities and preserved mitochondrial mass and energy production. In cultured podocytes and tubular cells, C3a caused altered mitochondrial fragmentation and distribution, and reduced anti-oxidant SOD2 activity. Stx2 potentiated the responsiveness of renal cells to the detrimental effects of C3a through increased C3aR protein expression. These results indicate that C3aR may represent a novel target in Stx-associated HUS for the preservation of renal cell integrity through the maintenance of mitochondrial function.</p>
Data for PNASnexus article Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell phenotype
<p>Adult salivary stem/progenitor cells (SSPC) have an intrinsic property to self-renew in order to maintain tissue architecture and homeostasis. Adult salivary glands have been documented to harbor SSPC, which have been shown to play a vital role in the regeneration of the glandular structures post radiation damage. We have previously demonstrated that activation of aldehyde dehydrogenase 3A1 (ALDH3A1) after radiation reduced aldehyde accumulation in SSPC, leading to less apoptosis and improved salivary function. We subsequently found that sustained pharmacological ALDH3A1 activation is critical to enhance regeneration of murine submandibular gland after radiation damage. Further investigation shows that ALDH3A1 function is crucial for SSPC self-renewal and survival even in the absence of radiation stress. Salivary glands from <em>Aldh3a1</em>-null mice have fewer acinar structures than wildtype mice. ALDH3A1 deletion or pharmacological inhibition in SSPC leads to a decrease in mitochondrial DNA copy number, lower expression of mitochondrial specific genes and proteins, structural abnormalities, lower membrane potential, and reduced cellular respiration. Loss or inhibition of ALDH3A1 also elevates ROS levels and accumulation of ALDH3A1 substrate 4-hydroxynonenal (4-HNE, a lipid peroxidation product), leading to decreased survival of murine SSPC that can be rescued by treatment with 4-HNE specific carbonyl scavengers. Our data indicate that ALDH3A1 activity protects mitochondrial function and is important for the regeneration activity of SSPC. This knowledge will help to guide our translational strategy of applying ALDH3A1 activators in the clinic to prevent radiation-related hyposalivation in head and neck cancer patients.</p>
Study of Dapagliflozin on Mitochondrial Dysfunction and Impaired Insulin Signaling/Action
ClinicalTrials.gov study NCT01439854. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Atypical Antipsychotic-induced Mitochondrial Dysfunction in Patients With Schizophrenia
ClinicalTrials.gov study NCT06236451. IPD Sharing: YES. Countries: 1. Publications: 11.
Data for: Mitochondrial Ca2+-coupled generation of reactive oxygen species, peroxynitrite formation, and endothelial dysfunction in Cantú syndrome
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Data for PNASnexus article Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell phenotype
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GSDMD-mediated mitochondrial dysfunction in marginal cells: A potential driver of inflammation and stria vascularis damage in CIHL
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Human-derived fecal microbiota transplantation alleviates mitochondrial dysfunction and social deficits in the BTBR mouse model for autism
<p><span><span>Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by social communication deficiencies and stereotypic behaviors influenced by hereditary and/or environmental risk factors. There are currently no approved medications for treating the core symptoms of ASD. Human fecal microbiota transplantation (FMT) has emerged as a potential intervention to improve autistic symptoms, but the underlying mechanisms are not fully understood. </span></span><span><span><span><span>In this study, we evaluated the effects of human-derived FMT on behavioral and multi-omics profiles of the BTBR mice, an established model for ASD. FMT effectively alleviated the social deficits in the BTBR mice and normalized their distinct plasma metabolic profile, notably reducing the elevated long-chain acylcarnitines. Integrative analysis linked these phenotypic changes to specific <em>Bacteroides</em> species and vitamin B<sub>6</sub> metabolism. Indeed, vitamin B<sub>6</sub> supplementation improved the social behaviors in BTBR mice. Collectively, these findings shed new light on the interplay between FMT and vitamin B<sub>6</sub> metabolism and revealed a potential mechanism underlying the therapeutic role of FMT in ASD.</span></span></span></span></p>
Study On the Role of Mitochondrial Dysfunction in the Pathogenesis of Metformin-associated Lactic Acidosis
ClinicalTrials.gov study NCT00942123. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Gastrointestinal Dysfunction in Children Affected With Mitochondrial Disorders
ClinicalTrials.gov study NCT01137240. IPD Sharing: Not stated. Countries: 1. Publications: 3.
The Impact of Mitochondrial Dysfunction on Human Bone Cell Metabolism and Remodelling
ClinicalTrials.gov study NCT05483738. IPD Sharing: NO. Countries: 1. Publications: 31.
Mitochondrial Dysfunctions Driving Insulin Resistance
ClinicalTrials.gov study NCT06080581. IPD Sharing: NO. Countries: 1. Publications: 15.
Combined Antioxidant Therapy on Oxidative Stress, Mitochondrial Dysfunction Markers in Diabetic Retinopathy
ClinicalTrials.gov study NCT03702374. IPD Sharing: NO. Countries: 1. Publications: 6.
MitoQ for Early-phase Schizophrenia-spectrum Disorder and Mitochondrial Dysfunction
ClinicalTrials.gov study NCT06191965. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Evaluation of Mitochondrial Dysfunction in Severe Burn and Trauma Patients
ClinicalTrials.gov study NCT01812941. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Mitochondrial Dysfunction in Trauma-related Coagulopathy
ClinicalTrials.gov study NCT05004844. IPD Sharing: NO. Countries: 1. Publications: 5.
Mitochondrial Dysfunction of Alveolar and Circulating Immune Cells During Acute Respiratory Distress Syndrome: Impact of Infectious Aggression and Alveolar Stretching as a Result of Mechanical Ventila
ClinicalTrials.gov study NCT03955887. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Beneficial Effects of Coenzyme Q10 Treatment on the Mitochondrial Dysfunction and Oxidative Stress Associated to Atherothrombosis Developement in Antiphospholipidid Syndrome Patients
ClinicalTrials.gov study NCT02218476. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Ataxia-telangiectasia: Treating Mitochondrial Dysfunction With Nicotinamide Riboside
ClinicalTrials.gov study NCT06324877. IPD Sharing: NO. Countries: 1. Publications: 27.
Mitochondrial Dysfunction in the Pathophysiology and Treatment of Bipolar Disorder
ClinicalTrials.gov study NCT00327756. IPD Sharing: Not stated. Countries: 1. Publications: 3.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.