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Mitochondria importance articles
Abstract-level scientific briefs on mitochondria preprints—structured for researchers and agents. Free in the browser. Machine JSON remains available via x402 for bots.
23 of 77 articles · updated 2026-08-08T16:01Z
- biorxiv2026-08-04score 93mitophagyOXPHOSredox biology
The effect of melittin intervention on murine cervical cancer cells: An in-depth proteomics investigation
Scientific focus: mitophagy, OXPHOS, redox biology, metabolism. Core claim (from abstract): Melittin significantly inhibited the migration and invasion of U14 cervical cancer cells and increased cell death. Dysfunction linkage: oxidative stress; reactive oxygen species; cell death; mitophagy. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: The effect of melittin intervention on murine cervical cancer cells: An in-depth proteomics investigation
- biorxiv2026-08-03score 93redox biologymetabolismimmunology
Activation of the NAD⁺–Sirtuin Axis Protects Against Chronic Doxorubicin-Induced Subclinical Renal Tubular Injury Through Restoration of…
Scientific focus: redox biology, metabolism, immunology, cancer. Core claim (from abstract): We investigated whether chronic low-dose DOX exposure induces persistent mitochondrial dysfunction in renal tubules and evaluated the therapeutic potential of activating the NAD⁺–Sirtuin axis. Dysfunction linkage: mitochondrial dysfunction; functional impairment; oxidative stress; inflammation. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Activation of the NAD⁺–Sirtuin Axis Protects Against Chronic Doxorubicin-Induced Subclinical Renal Tubular Injury Through Restoration of Mitochondrial Homeostasis and Suppression of Inflammation
- medrxiv2026-08-06score 86OXPHOSmetabolismtherapeutics
GLP-1 Refractory Obesity Is Associated with Inferior Weight Loss After Bariatric Surgery and a Distinct Hepatic Mitochondrial Phenotype
Scientific focus: OXPHOS, metabolism, therapeutics, structural biology. Core claim (from abstract): Objectives To characterize the hepatic histological, ultrastructural, and molecular phenotype of GRO at bariatric surgery, determine its recovery following surgery, and identify preoperative hepatic biomarkers associated with postoperative weight loss. Dysfunction linkage: mitochondrial dysfunction; OXPHOS / ETC; disease context; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: GLP-1 Refractory Obesity Is Associated with Inferior Weight Loss After Bariatric Surgery and a Distinct Hepatic Mitochondrial Phenotype
- biorxiv2026-07-31score 83redox biologymetabolismtherapeutics
Metformin enhances differentiation and function of skeletal muscle in models of Facioscapulohumeral Muscular Dystrophy (FSHD)
Scientific focus: redox biology, metabolism, therapeutics, computational. Core claim (from abstract): Metabolic perturbation, mitochondrial dysfunction, and oxidative stress are key contributors to FSHD pathology. Dysfunction linkage: mitochondrial dysfunction; oxidative stress; reactive oxygen species; disease context. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Metformin enhances differentiation and function of skeletal muscle in models of Facioscapulohumeral Muscular Dystrophy (FSHD)
- biorxiv2026-08-03score 82mitochondrial dynamicsredox biologymetabolism
Mitochondrial and protein homeostasis pathways are transcriptionally impaired in islets during type 1 diabetes pathogenesis
Scientific focus: mitochondrial dynamics, redox biology, metabolism, immunology. Core claim (from abstract): In pancreas tissue from donors across the natural history of T1D, we utilized an in-situ, whole - islet phenotypical and transcriptomic approach to unravel novel targets in the glucose-stimulus coupled secretion pathway that are similarly impaired in T-cell infiltrated and non-infiltrated islets. Dysfunction linkage: mitochondrial dysfunction; functional impairment; bioenergetics; disease context. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Mitochondrial and protein homeostasis pathways are transcriptionally impaired in islets during type 1 diabetes pathogenesis
- biorxiv2026-08-04score 78apoptosismetabolismimmunology
Gut-Associated Metabolites (GAMs) revitalize dysfunctional CD8⁺ T lymphocytes in Osteosarcoma
Scientific focus: apoptosis, metabolism, immunology, cancer. Core claim (from abstract): Here we report that peripheral CD8⁺ T lymphocytes in osteosarcoma patients are less frequent in circulation, hypo-producers of effector cytokines (IFN-γ and TNF-α), and have compromised metabolic fitness․ We characterized and investigated the effect of a panel of microbiota-derived GAMs on CD8⁺ T lymphocytes, confirming their immunomodulatory role with respect to CD8⁺ T lymphocytes activation, cellular metabolism and effector functions․ Indole-3-lactic acid (ILA; product of tryptophan metabolism), was observed to be the strongest immunostimulant among all the GAMs studied. Dysfunction linkage: mitochondrial dysfunction; functional impairment; cell death; cancer. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Gut-Associated Metabolites (GAMs) revitalize dysfunctional CD8⁺ T lymphocytes in Osteosarcoma
- biorxiv2026-08-04score 77OXPHOSbiogenesismetabolism
FAM136A is an essential chaperone for mitochondrial membrane protein biogenesis
Scientific focus: OXPHOS, biogenesis, metabolism, genetics. Core claim (from abstract): ABSTRACT The metabolic and signaling function of mitochondria rely on a network of chaperones within the inner membrane space (IMS) that regulate the biogenesis of nascent mitochondrial proteins. Dysfunction linkage: OXPHOS / ETC; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: FAM136A is an essential chaperone for mitochondrial membrane protein biogenesis
- biorxiv2026-08-04score 76metabolismneurobiology
A guanosine metabolism-bioenergetics intersection drives Parkinson’s disease
Scientific focus: metabolism, neurobiology. Core claim (from abstract): We show here that the reliance on these two purine-based metabolites intersect at another PD susceptibility gene that encodes nucleoside diphosphate kinase (NDK) which converts ATP into GTP. Dysfunction linkage: mitochondrial dysfunction; functional impairment; bioenergetics; disease context. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: A guanosine metabolism-bioenergetics intersection drives Parkinson’s disease
- biorxiv2026-08-01score 76mitophagyredox biologymetabolism
Combinatorial sequence elements fine-tune mitochondrial protein import to facilitate dual localization
Scientific focus: mitophagy, redox biology, metabolism. Core claim (from abstract): Here, we identify multiple sequence elements that compromise the matrix localization of the phosphatase PPTC7 to facilitate its accumulation at the outer mitochondrial membrane (OMM), where it regulates mitophagy. Dysfunction linkage: mitophagy. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Combinatorial sequence elements fine-tune mitochondrial protein import to facilitate dual localization
- biorxiv2026-07-31score 76OXPHOSredox biologymetabolism
Loss of neurofibromin alters adult metabolism via effects during a developmental critical period
Scientific focus: OXPHOS, redox biology, metabolism, neurobiology. Core claim (from abstract): Neurofibromatosis type 1 (OMIM 162200) is a genetic disorder that results from mutations in the NF1 gene and its encoded neurofibromin protein (Nf1). Dysfunction linkage: OXPHOS / ETC; disease context; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Loss of neurofibromin alters adult metabolism via effects during a developmental critical period
- biorxiv2026-08-05score 75redox biologymetabolismcancer
Endocytosis of ALK promotes glucose uptake in ALK -amplified neuroblastoma
Scientific focus: redox biology, metabolism, cancer, genetics. Core claim (from abstract): We recently identified a noncanonical mechanism in which RTK-containing endocytic vesicles deliver extracellular glucose to hexokinases associated with the outer mitochondrial membrane, thereby promoting cellular glucose uptake. Dysfunction linkage: functional impairment; cancer; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Endocytosis of ALK promotes glucose uptake in ALK -amplified neuroblastoma
- biorxiv2026-07-31score 75redox biologymetabolismcomputational
Restoration of Redox Homeostasis and Endogenous Aldehyde Detoxification by UT-018 Following Acute Ethanol Exposure
Scientific focus: redox biology, metabolism, computational. Core claim (from abstract): Oxidation of ethanol by alcohol dehydrogenase (ADH) consumes nicotinamide adenine dinucleotide (NAD) while generating NADH, shifting the intracellular redox state toward a highly reduced environment that impairs mitochondrial function, limits endogenous aldehyde dehydrogenase (ALDH)-mediated acetaldehyde clearance, and promotes oxidative stress and tissue injury. Dysfunction linkage: functional impairment; oxidative stress; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.
Source preprint: Restoration of Redox Homeostasis and Endogenous Aldehyde Detoxification by UT-018 Following Acute Ethanol Exposure
- biorxiv2026-07-31score 73redox biologymetabolismneurobiology
A Grape Seed Oligomeric Procyanidin Extract Reverses Diet-Induced Obesity Through Gut Microbiota Remodeling and Restoration of GLP-1, Gut…
Scientific focus: redox biology, metabolism, neurobiology, immunology. Core claim (from abstract): Background Obesity is a complex multifactorial disease associated with chronic low grade inflammation, gut microbiota dysbiosis, and impaired gut-brain communication. Dysfunction linkage: functional impairment; disease context; inflammation; systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: A Grape Seed Oligomeric Procyanidin Extract Reverses Diet-Induced Obesity Through Gut Microbiota Remodeling and Restoration of GLP-1, Gut-Brain, and Gut-Liver Signaling
- biorxiv2026-08-04score 72apoptosisredox biologymetabolism
SAMHD1 enhances HIV-1-induced glycolysis in monocytic cells through hexokinase 2 upregulation
Scientific focus: apoptosis, redox biology, metabolism, immunology. Core claim (from abstract): Building on our previous finding that SAMHD1 promotes mitochondrial membrane damage in HIV-1-infected monocytic cells, here we identify a new function for SAMHD1 in enhancing HIV-1-induced glycolysis through upregulation of hexokinase 2 (HK2). Dysfunction linkage: organelle damage; oxidative stress; reactive oxygen species; cell death. Moderate priority: useful for specialists in the listed topics.
Source preprint: SAMHD1 enhances HIV-1-induced glycolysis in monocytic cells through hexokinase 2 upregulation
- biorxiv2026-08-04score 67metabolismagingstructural biology
A single Omicron mutation reshapes ORF3a-driven host-cell remodelling
Scientific focus: metabolism, aging, structural biology, computational. Core claim (from abstract): Here, we combine complementary imaging approaches to define ORF3a function at nanometric scale, identifying underlying mechanisms, and determining how Omicron variant rewire this activity. Dysfunction linkage: aging; systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: A single Omicron mutation reshapes ORF3a-driven host-cell remodelling
- biorxiv2026-08-06score 66mitochondrial dynamicsredox biologymetabolism
A Multiscale Computational Framework for the Mg-28 Radio-Cofactor Hypothesis
Scientific focus: mitochondrial dynamics, redox biology, metabolism, cancer. Core claim (from abstract): Enzymatic cofactors occupy a uniquely fundamental position within this architecture: they enable catalytic activity itself. Dysfunction linkage: cancer; systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: A Multiscale Computational Framework for the Mg-28 Radio-Cofactor Hypothesis: Conditional Emergence of Coordinated Disruption under the Gate Condition
- biorxiv2026-08-04score 66mitochondrial dynamicsredox biologymetabolism
Deep-ultraviolet microscopy reveals biomolecular spatiotemporal intracellular dynamics
Scientific focus: mitochondrial dynamics, redox biology, metabolism, aging. Core claim (from abstract): In this work, we demonstrate deep-ultraviolet (UV) microscopy as a powerful, label-free, high-resolution approach for quantifying multiscale intracellular dynamics with biomolecular specificity. Dysfunction linkage: disease context; aging; systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: Deep-ultraviolet microscopy reveals biomolecular spatiotemporal intracellular dynamics
- biorxiv2026-08-04score 66mitochondrial dynamicsmetabolism
A Modular Platform for Purification of Organelle-associated Mitochondria Reveals Functional Specialization at Organelle Contact Sites
Scientific focus: mitochondrial dynamics, metabolism. Core claim (from abstract): Organelle contact sites are spatially restricted hubs that regulate mitochondrial metabolism, signaling, and dynamics, and are therefore well positioned to influence mitochondrial specialization. Dysfunction linkage: systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: A Modular Platform for Purification of Organelle-associated Mitochondria Reveals Functional Specialization at Organelle Contact Sites
- biorxiv2026-08-04score 65redox biologymetabolismcomputational
Non-Invasive Embryo Quality Assessment via Matrix-Optimized Untargeted LC-MS Metabolomics of Spent Embryo Culture Media and Weighted Ense…
Scientific focus: redox biology, metabolism, computational. Core claim (from abstract): Results We systematically optimized sample preparation for untargeted LC-MS metabolomics of SECM using human serum as a reference. Dysfunction linkage: systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: Non-Invasive Embryo Quality Assessment via Matrix-Optimized Untargeted LC-MS Metabolomics of Spent Embryo Culture Media and Weighted Ensemble Machine Learning
- medrxiv2026-07-31score 65redox biologymetabolismtherapeutics
TruBlk TM Shilajit Resin Supplementation Improves Muscle Strength, Endurance, and Exercise Recovery in Males Undertaking Resistance Train…
Scientific focus: redox biology, metabolism, therapeutics. Core claim (from abstract): Prior controlled trials have demonstrated increases in testosterone and retention of muscular strength with purified shilajit, though large trials in resistance-trained populations have been absent. Dysfunction linkage: organelle damage. Moderate priority: useful for specialists in the listed topics.
Source preprint: TruBlk™ Shilajit Resin Supplementation Improves Muscle Strength, Endurance, and Exercise Recovery in Males Undertaking Resistance Training: A Randomised, Double-Blind, Placebo-Controlled, Multicenter Trial
- biorxiv2026-08-04score 64metabolismimmunology
Decoding EGFR ligand bias through an endocytic organelle platform
Scientific focus: metabolism, immunology. Core claim (from abstract): Here, we identify a receptor-proximal mechanism that links ligand-specific EGFR activation to distinct endocytic and biological outputs. Dysfunction linkage: systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: Decoding EGFR ligand bias through an endocytic organelle platform
- biorxiv2026-08-01score 64redox biologymetabolismneurobiology
Cross-species neural co-culture uncovers metabolic signatures of cellular crosstalk
Scientific focus: redox biology, metabolism, neurobiology, immunology. Core claim (from abstract): This increase in brain size evolved alongside advanced cognitive abilities as well as an elevated energetic demand. Dysfunction linkage: systemic metabolic stress. Moderate priority: useful for specialists in the listed topics.
Source preprint: Cross-species neural co-culture uncovers metabolic signatures of cellular crosstalk
- biorxiv2026-08-05score 48metabolismstructural biologycomputational
A proximity biotinylation approach for the identification of membrane contact site proteins in Toxoplasma gondii
Scientific focus: metabolism, structural biology, computational. Core claim (from abstract): Yet, little is known about the makeup or function of their MCSs, leaving a gap in our understanding of how organelles communicate beyond conventional model eukaryotes. Dysfunction linkage: disease context. Lower priority within the current window unless the topic matches a narrow research focus.
Source preprint: A proximity biotinylation approach for the identification of membrane contact site proteins in Toxoplasma gondii