Results 101 to 110 of about 17,663,383 (215)

Fetal glucose availability: a key regulator of the metabolic, hormonal and contractility profiles of the fetal sheep heart

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend To investigate the role of glucose availability in fetal left ventricle (LV) development, this study assessed whether maternal late gestation undernutrition (LGUN; 50% of Control diet) induced alterations in the contractility, metabolic, and hormonal profile can be ameliorated in LGUN fetuses receiving glucose infusion (LGUN+G ...
Melanie R. Bertossa   +10 more
wiley   +1 more source

Autophagy in ischemic aged livers

open access: yesLiver Research, 2018
Ischemia/reperfusion (I/R) injury inevitably occurs during liver resection and transplantation. Elderly patients poorly recover from these surgeries.
Choonghee Lee, Jae-Sung Kim
doaj   +1 more source

Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The capillary–mitochondria–ion channel (CMIC) axis scales structural resources to match functional workload. (Left) In settings of restricted energetic capacity (e.g. cortical neurons), sparse capillary networks and modest mitochondrial pools set a lower energetic ceiling, sufficient to support phasic, low‐workload excitability. (
L. Fernando Santana, Scott Earley
wiley   +1 more source

Demonstration of beat‐to‐beat, on‐demand ATP synthesis in ventricular myocytes reveals sex‐specific mitochondrial and cytosolic dynamics

open access: yesThe Journal of Physiology, EarlyView.
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

Loss of Mfn1 but not Mfn2 enhances adipogenesis.

open access: yesPLoS ONE
ObjectiveA biallelic missense mutation in mitofusin 2 (MFN2) causes multiple symmetric lipomatosis and partial lipodystrophy, implicating disruption of mitochondrial fusion or interaction with other organelles in adipocyte differentiation, growth and/or ...
Jake P Mann   +15 more
doaj   +1 more source

SARS‐CoV‐2 targets mitochondria, exacerbating COVID‐19 pneumonia

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Following entry into airway epithelial cells (AECs), SARS‐CoV‐2 releases its single‐stranded RNA into the cytoplasm, where it is translated into viral proteins. Several of these viral proteins localize to mitochondria and interact with key mitochondrial components.
Danchen Wu   +5 more
wiley   +1 more source

Structural insights of human mitofusin-2 into mitochondrial fusion and CMT2A onset

open access: yesNature Communications, 2019
Mitofusin-2 (MFN2) is a dynamin-like GTPase that plays a central role in regulating mitochondrial fusion and cell metabolism. Here, authors report crystal structures of truncated human MFN2 in different nucleotide-loading states and show that MFN2 forms ...
Yu-Jie Li   +15 more
doaj   +1 more source

Charcot-Marie-Tooth neuropathy type 2A: novel mutations in the mitofusin 2 gene (MFN2)

open access: yesBMC Medical Genetics, 2006
Background Charcot-Marie-Tooth neuropathies are a group of genetically heterogeneous diseases of the peripheral nervous system. Mutations in the MFN2 gene have been reported as the primary cause of Charcot-Marie-Tooth disease type 2A.
Haas Gerhard   +6 more
doaj   +1 more source

Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions

open access: yesThe Journal of Pathology, Volume 269, Issue 3, Page 268-283, July 2026.
Abstract Endoplasmic reticulum stress (ERS) occurs when the protein‐folding capacity of the endoplasmic reticulum (ER) is overwhelmed, triggering the unfolded protein response (UPR) to restore homeostasis. However, severe or persistent ERS can shift the UPR toward pro‐inflammatory, apoptotic, and fibrotic signaling, thereby exacerbating tissue injury ...
Lanlan Song   +6 more
wiley   +1 more source

Linking neurogenesis, oligodendrogenesis, and myelination defects to neurodevelopmental disruption in primary mitochondrial disorders

open access: yesFEBS Letters, Volume 600, Issue 12, Page 1699-1716, June 2026.
Mitochondrial remodeling shapes neural and glial lineage progression by matching metabolic supply with demand. Elevated OXPHOS supports differentiation and myelin formation, while myelin compaction lowers mitochondrial dependence, revealing mitochondria as key drivers of developmental energy adaptation.
Sahitya Ranjan Biswas   +3 more
wiley   +1 more source

Home - About - Disclaimer - Privacy