[HTML][HTML] Mitochondria–lysosome crosstalk: from physiology to neurodegeneration

CM Deus, KF Yambire, PJ Oliveira… - Trends in molecular …, 2020 - cell.com
Cellular function requires coordination between different organelles and metabolic cues.
Mitochondria and lysosomes are essential for cellular metabolism as major contributors of …

[HTML][HTML] Molecular neurobiology of mTOR

K Switon, K Kotulska, A Janusz-Kaminska… - Neuroscience, 2017 - Elsevier
Mammalian/mechanistic target of rapamycin (mTOR) is a serine-threonine kinase that
controls several important aspects of mammalian cell function. mTOR activity is modulated …

Metabolic reprogramming during neuronal differentiation from aerobic glycolysis to neuronal oxidative phosphorylation

X Zheng, L Boyer, M **, J Mertens, Y Kim, L Ma, L Ma… - elife, 2016 - elifesciences.org
How metabolism is reprogrammed during neuronal differentiation is unknown. We found that
the loss of hexokinase (HK2) and lactate dehydrogenase (LDHA) expression, together with …

mTORC1 regulates mitochondrial integrated stress response and mitochondrial myopathy progression

NA Khan, J Nikkanen, S Yatsuga, C Jackson, L Wang… - Cell metabolism, 2017 - cell.com
Mitochondrial dysfunction elicits various stress responses in different model systems, but
how these responses relate to each other and contribute to mitochondrial disease has …

Serine catabolism feeds NADH when respiration is impaired

L Yang, JCG Canaveras, Z Chen, L Wang, L Liang… - Cell metabolism, 2020 - cell.com
NADH provides electrons for aerobic ATP production. In cells deprived of oxygen or with
impaired electron transport chain activity, NADH accumulation can be toxic. To minimize …

[HTML][HTML] Glycerol-3-phosphate biosynthesis regenerates cytosolic NAD+ to alleviate mitochondrial disease

S Liu, S Fu, G Wang, YU Cao, L Li, X Li, J Yang, N Li… - Cell metabolism, 2021 - cell.com
Electron transport chain (ETC) dysfunction or hypoxia causes toxic NADH accumulation.
How cells regenerate NAD+ under such conditions remains elusive. Here, integrating …

Defective metabolic programming impairs early neuronal morphogenesis in neural cultures and an organoid model of Leigh syndrome

G Inak, A Rybak-Wolf, P Lisowski, TM Pentimalli… - Nature …, 2021 - nature.com
Leigh syndrome (LS) is a severe manifestation of mitochondrial disease in children and is
currently incurable. The lack of effective models hampers our understanding of the …

Disturbed glucose and pyruvate metabolism in glaucoma with neuroprotection by pyruvate or rapamycin

JM Harder, C Guymer, JPM Wood… - Proceedings of the …, 2020 - National Acad Sciences
Intraocular pressure-sensitive retinal ganglion cell degeneration is a hallmark of glaucoma,
the leading cause of irreversible blindness. Here, we used RNA-sequencing and …

Impaired mitochondrial dynamics and mitophagy in neuronal models of tuberous sclerosis complex

D Ebrahimi-Fakhari, A Saffari, L Wahlster, A Di Nardo… - Cell reports, 2016 - cell.com
Tuberous sclerosis complex (TSC) is a neurodevelopmental disease caused by TSC1 or
TSC2 mutations and subsequent activation of the mTORC1 kinase. Upon mTORC1 …

Mitochondrial dysfunction and neurodegeneration in lysosomal storage disorders

N Plotegher, MR Duchen - Trends in molecular medicine, 2017 - cell.com
Lysosomal storage disorders (LSDs) are rare inherited debilitating and often fatal disorders.
Caused by mutations affecting lysosomal proteins, LSDs are characterized by the …