Results 121 to 130 of about 22,170 (231)

Overexpression of Optic Atrophy Type 1 Protects Retinal Ganglion Cells and Upregulates Parkin Expression in Experimental Glaucoma

open access: yesFrontiers in Molecular Neuroscience, 2018
Glaucoma is a neurodegenerative disease that features progressive loss of retinal ganglion cells (RGCs). Increasing evidences have revealed that impaired mitochondrial dynamics occurs early in neurodegenerative diseases.
Xinxin Hu   +19 more
doaj   +1 more source

Harnessing energy metabolism for enhanced bone defect repair: Mechanisms and therapeutic strategies

open access: yesVIEW, EarlyView.
This review addresses the critical challenge of bone defect repair by focusing on the underexplored role of cellular energy metabolism. It synthesizes regulatory mechanisms in bone‐forming cells and sums up innovative strategies—leveraging cell derivatives, active factors, and biomimetic scaffolds—to modulate metabolism for enhanced regeneration.
Junting Li   +5 more
wiley   +1 more source

A Splicing Mutation in the Novel Mitochondrial Protein DNAJC11 Causes Motor Neuron Pathology Associated with Cristae Disorganization, and Lymphoid Abnormalities in Mice [PDF]

open access: yes, 2014
Mitochondrial structure and function is emerging as a major contributor to neuromuscular disease, highlighting the need for the complete elucidation of the underlying molecular and pathophysiological mechanisms. Following a forward genetics approach with
Douni, E   +9 more
core   +1 more source

The long and short of OPA1 [PDF]

open access: yesJournal of Cell Biology, 2016
![Figure][1] Neurons from mice lacking prohibitin 2 and OMA1 carry huge mitochondria that lack cristae. OMA1 promotes neurodegeneration by tipping the balance between mitochondrial fusion and fission, [Korwitz et al.][2] reveal.
openaire   +1 more source

Mechanical Force Promotes Mitochondrial Transfer From Macrophages to BMSCs to Enhance Bone Formation

open access: yesCell Proliferation, EarlyView.
Mechanical tension activates Drp1‐mediated mitochondrial fission in macrophages, facilitating the release of Mito‐EVs that are subsequently transferred to BMSCs. Additionally, the CD200R‐CD200 interaction enhances the uptake of these mechanically stimulated macrophage‐derived Mito‐EVs by BMSCs, ultimately promoting osteogenic differentiation.
Yingyi Li   +8 more
wiley   +1 more source

Non\u2011syndromic isolated dominant optic atrophy caused by the p.R468C mutation in the AFG3 like matrix AAA peptidase subunit 2 gene [PDF]

open access: yes, 2017
Autosomal dominant optic atrophy (DOA) is the most frequent form of hereditary optic atrophy, a disease presenting with considerable inter- and intra-familial clinical variability.
Colavito, Davide   +9 more
core   +1 more source

Growth differentiation factor 15 mitigates lipotoxic steatosis by preserving mitochondrial morphodynamics and augmenting fatty acid oxidation in hepatocytes and liver organoids

open access: yesDiabetes, Obesity and Metabolism, EarlyView.
Abstract Aims Growth differentiation factor 15 (GDF15) has emerged as a promising metabolic regulator with hepatoprotective properties in metabolic dysfunction‐associated steatotic liver disease (MASLD), yet its underlying mechanisms remain elusive.
Jia Li   +9 more
wiley   +1 more source

Assessing the effects of mitofusin 2 deficiency in the adult heart using 3D electron tomography [PDF]

open access: yes, 2017
The effects of mitofusin 2 (MFN2) deficiency, on mitochondrial morphology and the mitochondria-junctional sarcoplasmic reticulum (jSR) complex in the adult heart, have been previously investigated using 2D electron microscopy, an approach which is unable
Cabrera-Fuentes, Hector   +12 more
core   +2 more sources

OPA1 and mitochondrial solute carriers in bioenergetic metabolism [PDF]

open access: yesMolecular & Cellular Oncology, 2015
The mitochondrial fusion protein optic atrophy 1 (OPA1) is required to maintain cristae structure and for ATP synthase assembly. Our recent work demonstrates that OPA1 dynamically regulates these processes by sensing changes in nutrient availability through mitochondrial solute carriers and adjusting the metabolic output of mitochondria accordingly ...
openaire   +2 more sources

ER proteostasis meets mitochondrial function: contact sites as hubs of communication and therapeutic targets

open access: yesThe FEBS Journal, EarlyView.
Proteostasis ensures proper protein folding, modification, and degradation, while its impairment triggers ER stress. Chronic ER stress and maladaptive UPR via the CHOP–ERO1 axis remodel ERMCs, altering calcium signaling and mitochondrial metabolism.
Giorgia Maria Renna   +5 more
wiley   +1 more source

Home - About - Disclaimer - Privacy