Results 41 to 50 of about 9,347 (172)
Properties of the permeability transition in VDAC1−/− mitochondria
Opening of the permeability transition pore (PTP), a high-conductance mitochondrial channel, causes mitochondrial dysfunction with Ca2+ deregulation, ATP depletion, release of pyridine nucleotides and of mitochondrial apoptogenic proteins. Despite major efforts, the molecular nature of the PTP remains elusive.
KRAUSKOPF A +4 more
openaire +3 more sources
Expression profiling of mitochondrial voltage-dependent anion channel-1 associated genes predicts recurrence-free survival in human carcinomas. [PDF]
Mitochondrial voltage-dependent anion channels (VDACs) play a key role in mitochondria-mediated apoptosis. Both in vivo and in vitro evidences indicate that VDACs are actively involved in tumor progression.
Jae-Hong Ko +4 more
doaj +1 more source
Deletion of VDAC1 Hinders Recovery of Mitochondrial and Renal Functions After Acute Kidney Injury
Voltage-dependent anion channels (VDACs) constitute major transporters mediating bidirectional movement of solutes between cytoplasm and mitochondria.
Grazyna Nowak +2 more
doaj +1 more source
Silencing VDAC1 Expression by siRNA Inhibits Cancer Cell Proliferation and Tumor Growth In Vivo
Alterations in cellular metabolism and bioenergetics are vital for cancer cell growth and motility. Here, the role of the mitochondrial protein voltage-dependent anion channel (VDAC1), a master gatekeeper regulating the flux of metabolites and ions ...
Tasleem Arif +4 more
doaj +1 more source
CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis
Ferroptosis is driven by mitochondrial permeability transition pore (mPTP) opening, which induces mitochondrial swelling and releases oxidized mitochondrial DNA. The released mtDNA activates cGAS–STING signaling, promotes ferritinophagy, and amplifies ferroptotic cell death. Disruption of mtDNA repair sensitizes tumors to ferroptosis in vivo, revealing
Hong Zhou +5 more
wiley +1 more source
xx xx. ABSTRACT Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by disrupted neuronal circuit maturation. Emerging evidence implicates microglial function and mitochondrial regulation as contributors to ASD‐associated biology, yet the mechanisms linking these processes to neuronal development remain poorly defined ...
Sydney P. Sterben +4 more
wiley +1 more source
Homoisoflavanone (HIF), a bioactive compound isolated from Polygonatum kingianum, selectively suppresses colorectal cancer progression by inducing DNA damage‐mediated mitochondrial apoptosis and parthanatos‐like cell death. HIF triggers mitochondrial dysfunction, including depolarized membrane potential, elevated ROS, and ATP depletion, while impairing
Hongjie Fan +12 more
wiley +1 more source
Targeted Mitochondrial ECSIT Overexpression Attenuates MASH by Increasing OTUD3 Expression
Mitochondrial ECSIT expression is reduced during MASH pathogenesis. Overexpression of mitochondrial ECSIT mitigates steatohepatitis and maintains hepatic metabolic homeostasis. Mechanistically, ECSIT enhances intramitochondrial OTUD3 expression to stabilize SIRT3 through deubiquitination, thus preserving mitochondrial function and impeding disease ...
Yuqing Jiang +11 more
wiley +1 more source
VDAC1 negatively regulates melanogenesis through the Ca 2+ -calcineurin-CRTC1-MITF pathway
This study revealed an important and novel role of mitochondrial VDAC1 in regulating melanogenesis in resting melanocytes through a Ca 2+ -regulated pathway that is independent of the alpha-MSH/UVB pathway.
Jianli Wang +4 more
doaj +1 more source
ABSTRACT Liver injury can lead to severe acute liver failure and even death in patients. Artesunate (ART), which is a derivative of artemisinin that has been approved by the FDA for the treatment of malaria, has significant regulatory effects on cell death and inflammation.
Zhe Zhang +17 more
wiley +1 more source

