Results 91 to 100 of about 10,788 (194)
Voltage-dependent anion channel1 (VDAC1) is a porin of the mitochondrial outer membrane that plays a very important role in the regulation of cellular metabolism and apoptosis. As a consequence of hypoxia (i.e.
Fabbri, Lucilla
core
Abstract figure legend Beat‐locked mitochondrial ATP transients reveal modular, sex‐specific bioenergetic control during excitation–contraction coupling. A, each action potential activates L‐type CaV1.2 channels, producing a Ca2+ influx that triggers ryanodine receptors (RyR2) and elicits SR Ca2+ release.
Paula Rhana +2 more
wiley +1 more source
Abstract figure legend This study used a non‐targeted proteomic approach to explore the skeletal muscle determinants of peak fat oxidation (PFO) and the exercise intensity at which this occurs (Fatmax). Comprehensive physiological phenotyping was completed in young, lean, physically active males, including blood and skeletal muscle sampling.
Eloise K. Tarry +11 more
wiley +1 more source
Ferroptosis is governed by the balance between reactive oxygen species (ROS)‐driven lipid peroxidation and a multi‐tiered antioxidant network. ROS sources include mitochondrial electron transport chain, voltage‐dependent anion channels, NADPH oxidases, and endoplasmic reticulum‐resident oxidoreductases, while antioxidant defenses span the primary GSH ...
Deepak K +5 more
wiley +1 more source
Is VDAC1 a Novel BCL2 Family Member that Binds BAX?
Apoptosis is a type of regulated cell death important for normal embryonic development and maintenance of adult tissues by removing excess or dysfunctional cells to ensure proper functioning of organs.
Pearson, Claire
core +1 more source
Prediction and biological analysis of yeast VDAC1 phosphorylation
The mitochondrial outer membrane protein porin 1 (Por1), the yeast orthologue of mammalian voltage-dependent anion channel (VDAC), is the major permeability pathway for the flux of metabolites and ions between cytosol and mitochondria. In yeast, several Por1 phosphorylation sites have been identified.
André D. Sousa +3 more
openaire +2 more sources
Both the misfolding of α-synuclein and mitochondrial dysfunction are considered two major contributors to Parkinson's disease (PD). However, the relationship between the two in normal and PD states remains unclear.
Yaping Chu +5 more
doaj +1 more source
Advances in the Core Role and Mechanisms of Mitochondrial Dysfunction in Alzheimer's Disease
In Alzheimer's disease, Aβ and Tau trigger mitochondrial dysfunction, driving a pathological cascade that results in cognitive decline. Gut microbiota dysbiosis exacerbates this via the gut–brain axis, making mitochondria a key therapeutic target. ABSTRACT Introduction Alzheimer's disease (AD) is a complex neurodegenerative disorder whose pathogenesis ...
Tianyi Gu +3 more
wiley +1 more source
Acylglycerol Kinase Inhibition Restores Mitophagy and Alleviates Alzheimer's Disease Pathology
AGK (acylglycerol kinase) is abnormally upregulated in AD patients and mouse models. By stabilizing the TOM–TIM complex, this excess AGK facilitates PINK1 translocation to the IMM and prevents its OMM accumulation, leading to mitophagy impairment.
Wensheng Li +12 more
wiley +1 more source
This study delivers dual key advances: mechanistically, we uncover a novel role of EGR1 as a pivotal transcriptional regulator that bridges upstream gene expression dysregulation to downstream mitophagic decline in oocyte aging; and translationally, we validate the therapeutic potential of the clinical drug UDCA to counteract oocyte aging.
Ying Zhang +5 more
wiley +1 more source

