Results 91 to 100 of about 60,467 (293)
This study demonstrates that dual UCP2/IL‐17 blockade reprograms T‐cell metabolism to overcome PDAC immunosuppression. Genipin‐mediated UCP2 inhibition enhances CD8⁺ T‐cell IFN‐γ via IL‐12R/STAT4/mTOR signaling and mitochondrial OXPHOS. Combined IL‐17 depletion amplifies Tc1/Th1 responses, reduces MDSCs, and prolongs survival in PDAC models ...
Chuan‐Teng Liu +11 more
wiley +1 more source
Increased liver content of DHA‐derived small lipid autacoids (i.e resolvin D1 and maresin 1) associates with enhanced mitochondrial oxidative phosphorylation, fatty acid β‐oxidation and bioenergetic metabolic flux. These features provide hepatic protection from steatotic, pro‐inflammatory and fibrogenic insults.
Cristina López‐Vicario +12 more
wiley +1 more source
PKM2 coordinates glycolysis with mitochondrial fusion and oxidative phosphorylation
A change in the metabolic flux of glucose from mitochondrial oxidative phosphorylation (OXPHOS) to aerobic glycolysis is regarded as one hallmark of cancer. However, the mechanisms underlying the metabolic switch between aerobic glycolysis and OXPHOS are
Tong Li +5 more
doaj +1 more source
Cytochrome c: Surfing Off of the Mitochondrial Membrane on the Tops of Complexes III and IV [PDF]
The proper arrangement of protein components within the respiratory electron transport chain is nowadays a matter of intense debate, since altering it leads to cell aging and other related pathologies.
Díaz Moreno, Irene +4 more
core +1 more source
Single‐Mitochondrion ATP Profiling Directs Discovery of Targetable OXPHOS Dependency in Cancers
MitoATP‐nFCM integrates nano‐flow cytometry with fluorogenic probes (ATP/membrane potential) and antibodies to quantify mitochondrial metabolites and protein expression at single‐organelle resolution, exposing oxidative phosphorylation (OXPHOS)‐driven metabolic rewiring in cancers.
Xu Xiao +7 more
wiley +1 more source
The NADPH oxidase NOX4 regulates redox and metabolic homeostasis preventing HCC progression
Loss of NOX4 in HCC tumor cells induces metabolic reprogramming in a Nrf2/MYC‐dependent manner to promote HCC progression. Abstract Background and Aims The NADPH oxidase NOX4 plays a tumor‐suppressor function in HCC. Silencing NOX4 confers higher proliferative and migratory capacity to HCC cells and increases their in vivo tumorigenic potential in ...
Irene Peñuelas‐Haro +14 more
wiley +1 more source
The ability to selectively eradicate oncogene-addicted tumors while reducing systemic toxicity has endeared targeted therapies as a treatment strategy. Nevertheless, development of acquired resistance limits the benefits and durability of such a regime ...
Jayshree Hirpara +10 more
doaj +1 more source
The interaction between trophoblasts and decidual polymorphonuclear myeloid‐derived suppressor cells (dPMN‐MDSCs) via the XCL1–XCR1 axis is crucial for fetal development during the third trimester. Disruption of this axis impairs FOXO1 activity and causes metabolic imbalance in dPMN‐MDSCs, contributing to adverse outcomes associated with advanced ...
Meiqi Chen +12 more
wiley +1 more source
RIPK3 dampens mitochondrial bioenergetics and lipid droplet dynamics in metabolic liver disease
RIPK3 dampens mitochondrial bioenergetics and lipid droplet dynamics in metabolic liver disease. Abstract Background and Aims Receptor‐interacting protein kinase 3 (RIPK3) mediates NAFLD progression, but its metabolic function is unclear. Here, we aimed to investigate the role of RIPK3 in modulating mitochondria function, coupled with lipid droplet (LD)
Marta B. Afonso +16 more
wiley +1 more source
Exercise training induces several skeletal muscle adaptations. Beta-guanidinopropionic acid (β-GPA) is a creatine analog that simulates the effect of exercise to induce mitochondrial biogenesis.
Fukao Naoki +4 more
doaj +1 more source

