Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation

Search Page

Filters

My NCBI Filters

Results by year

Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1987 1
1988 1
1991 2
1992 2
1993 10
1994 8
1995 15
1996 13
1997 15
1998 32
1999 39
2000 40
2001 35
2002 38
2003 36
2004 42
2005 35
2006 36
2007 45
2008 41
2009 55
2010 50
2011 39
2012 41
2013 45
2014 53
2015 53
2016 59
2017 55
2018 50
2019 50
2020 45
2021 57
2022 37
2023 35
2024 12

Text availability

Article attribute

Article type

Publication date

Search Results

1,087 results

Results by year

Filters applied: . Clear all
Page 1
Energy stress modulation of AMPK/FoxO3 signaling inhibits mitochondria-associated ferroptosis.
Zhong S, Chen W, Wang B, Gao C, Liu X, Song Y, Qi H, Liu H, Wu T, Wang R, Chen B. Zhong S, et al. Redox Biol. 2023 Jul;63:102760. doi: 10.1016/j.redox.2023.102760. Epub 2023 May 24. Redox Biol. 2023. PMID: 37267686 Free PMC article.
In addition, we identified a FDA-approved antipsychotic agent, the potent FoxO3a agonist trifluoperazine, which largely reduced ferroptosis-associated cerebral ischemia-reperfusion (CIR) injuries in rats through AMPK/FoxO3a/HIF-1alpha signaling and mitochondria-dependent m …
In addition, we identified a FDA-approved antipsychotic agent, the potent FoxO3a agonist trifluoperazine, which largely reduced ferroptosis- …
Excitotoxicity, calcium and mitochondria: a triad in synaptic neurodegeneration.
Verma M, Lizama BN, Chu CT. Verma M, et al. Transl Neurodegener. 2022 Jan 25;11(1):3. doi: 10.1186/s40035-021-00278-7. Transl Neurodegener. 2022. PMID: 35078537 Free PMC article. Review.
Glutamate is the most commonly engaged neurotransmitter in the mammalian central nervous system, acting to mediate excitatory neurotransmission. However, high levels of glutamatergic input elicit excitotoxicity, contributing to neuronal cell death following acute brain inj …
Glutamate is the most commonly engaged neurotransmitter in the mammalian central nervous system, acting to mediate excitatory neurotransmiss …
Pathophysiology of status epilepticus.
Walker MC. Walker MC. Neurosci Lett. 2018 Feb 22;667:84-91. doi: 10.1016/j.neulet.2016.12.044. Epub 2016 Dec 20. Neurosci Lett. 2018. PMID: 28011391 Review.
The latter enzyme plays a critical part in the generation of seizure-dependent reactive oxygen species. Calcium also accumulates in mitochondria resulting in mitochondrial failure (decreased ATP production), and opening of the mitochondrial permeability transition pore. .. …
The latter enzyme plays a critical part in the generation of seizure-dependent reactive oxygen species. Calcium also accumulates in mitoc …
Excitotoxicity and mitochondria.
Nicholls DG, Budd SL, Ward MW, Castilho RF. Nicholls DG, et al. Biochem Soc Symp. 1999;66:55-67. doi: 10.1042/bss0660055. Biochem Soc Symp. 1999. PMID: 10989657 Review.
Excitotoxicity is also implicated in a variety of slow neurodegenerative disorders. ...In contrast, DCD is irreversible. Elevated cytoplasmic calcium is not excitotoxic as long as mitochondria are depolarized; alternative substrates do not rescue cells about …
Excitotoxicity is also implicated in a variety of slow neurodegenerative disorders. ...In contrast, DCD is irreversible. Elevated cyt …
Neurotoxicity of Zinc.
Morris DR, Levenson CW. Morris DR, et al. Adv Neurobiol. 2017;18:303-312. doi: 10.1007/978-3-319-60189-2_15. Adv Neurobiol. 2017. PMID: 28889274 Review.
However, excess zinc, released after injury or disease, leads to excitotoxic neuronal death. The mechanisms of zinc-mediated neurotoxicity appear to include not only neuronal signaling but also regulation of mitochondrial function and energy production, as well as other me …
However, excess zinc, released after injury or disease, leads to excitotoxic neuronal death. The mechanisms of zinc-mediated neurotox …
Role of SIRT3 in mitochondrial biology and its therapeutic implications in neurodegenerative disorders.
Mishra Y, Kaundal RK. Mishra Y, et al. Drug Discov Today. 2023 Jun;28(6):103583. doi: 10.1016/j.drudis.2023.103583. Epub 2023 Apr 5. Drug Discov Today. 2023. PMID: 37028501 Review.
Reduced SIRT3 expression or activity causes hyperacetylation of hundreds of mitochondrial proteins, which has been linked with neurological abnormalities, neuro-excitotoxicity and neuronal cell death. A body of evidence has suggested, SIRT3 activation as a potential therap …
Reduced SIRT3 expression or activity causes hyperacetylation of hundreds of mitochondrial proteins, which has been linked with neurological …
Mitochondrial calcium at the synapse.
Datta S, Jaiswal M. Datta S, et al. Mitochondrion. 2021 Jul;59:135-153. doi: 10.1016/j.mito.2021.04.006. Epub 2021 Apr 23. Mitochondrion. 2021. PMID: 33895346 Review.
While increased ATP production is required during synaptic transmission, calcium buffering by mitochondria is crucial to prevent faulty neurotransmission and excitotoxicity. Interestingly, mitochondrial calcium also regulates the mobility of mitochondria with …
While increased ATP production is required during synaptic transmission, calcium buffering by mitochondria is crucial to prevent faul …
Cell Death Mechanisms of Neurodegeneration.
Fan J, Dawson TM, Dawson VL. Fan J, et al. Adv Neurobiol. 2017;15:403-425. doi: 10.1007/978-3-319-57193-5_16. Adv Neurobiol. 2017. PMID: 28674991 Review.
There are common mechanisms shared by genetically or pathologically distinct neurodegenerative diseases, such as excitotoxicity, mitochondrial deficits and oxidative stress, protein misfolding and translational dysfunction, autophagy and microglia activation. ...Besides ap …
There are common mechanisms shared by genetically or pathologically distinct neurodegenerative diseases, such as excitotoxicity, mito …
Mitochondrial SIRT3 and neurodegenerative brain disorders.
Anamika, Khanna A, Acharjee P, Acharjee A, Trigun SK. Anamika, et al. J Chem Neuroanat. 2019 Jan;95:43-53. doi: 10.1016/j.jchemneu.2017.11.009. Epub 2017 Nov 9. J Chem Neuroanat. 2019. PMID: 29129747 Review.
Out of seven homologues of Sirtuins identified in mammals, SIRT3, 4 & 5 have been found to be localized and active in mitochondria. During recent past, clusters of protein substrates for SIRT3 have been identified in mitochondria and thereby advocating SIRT3 as …
Out of seven homologues of Sirtuins identified in mammals, SIRT3, 4 & 5 have been found to be localized and active in mitochondria …
New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.
Zhang Z, Zhang A, Liu Y, Hu X, Fang Y, Wang X, Luo Y, Lenahan C, Chen S. Zhang Z, et al. Curr Neuropharmacol. 2022;20(7):1278-1296. doi: 10.2174/1570159X19666211101103646. Curr Neuropharmacol. 2022. PMID: 34720082 Free PMC article. Review.
Mitochondria are a double-membrane organelle, and they play an important role in energy production, cell growth, differentiation, apoptosis, and survival. ...In this review, we discuss the latest perspectives on the role of mitochondria in EBI and DCI after SAH. We …
Mitochondria are a double-membrane organelle, and they play an important role in energy production, cell growth, differentiation, apo …
1,087 results