Results 201 to 210 of about 26,946 (260)

Host–Microbe Mechanisms of Fusobacterium nucleatum in Colorectal Cancer

open access: yesMolecular Oral Microbiology, EarlyView.
Fusobacterium nucleatum and colorectal cancer. ABSTRACT The oral‐derived pathobiont Fusobacterium nucleatum has increasingly been implicated in colorectal cancer (CRC) progression through its ability to modulate inflammatory, immunological, and molecular pathways. F.
Hadda Lyzandra Austríaco Leite   +1 more
wiley   +1 more source

Understanding exosomes in diabetic wound healing

open access: yesPeriodontology 2000, EarlyView.
Abstract Background Diabetic wounds signify a major complication of diabetes mellitus, characterized by chronic inflammation, compromised angiogenesis, and high risk of infection, amputation, and mortality. Contemporary therapies remain limited in efficacy and durability.
Paras Ahmad   +4 more
wiley   +1 more source

Mitochondrial Ca2+ uniporter haploinsufficiency leads to sexually dimorphic redox imbalance and metabolic remodelling in the mouse brain

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The genetic inactivation of one Mcu allele leads to sex‐specific changes in neuronal function in adult mice, that is, the firing of action potentials and the relationship between cytosolic and mitochondrial Ca2+ levels. The ability to produce NAD(P)H by stimulated neural tissue is largely preserved in male mice but delayed in ...
Jenna Gray   +16 more
wiley   +1 more source

The role of extracellular vesicles in cell–cell crosstalk in cardiotoxicity

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Administration of a pharmacological agent can result in off‐target cardiotoxicity which can be driven by cell–cell crosstalk between healthy and dysfunctional cardiac cells. Extracellular vesicles (EVs) are lipid bilayer structures that can move biological cargo between cells, facilitating cell–cell crosstalk.
Gabriella Bachynskyj‐Bilas   +5 more
wiley   +1 more source

Excessive training does not induce mitochondrial dysfunction or impair insulin signalling within skeletal muscle

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Three weeks of overtraining in trained endurance athletes reduced exercise performance without impairing glucose tolerance. In skeletal muscle, overtraining was associated with increased expression of lipid metabolism‐related proteins, enhanced mitochondrial biogenesis and preserved insulin signalling, despite elevated oxidative ...
Geneviève J. DesOrmeaux   +7 more
wiley   +1 more source

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