Structure and Function of IP3Receptors DOI Open Access
David L. Prole, Colin W. Taylor

Cold Spring Harbor Perspectives in Biology, Journal Year: 2019, Volume and Issue: 11(4), P. a035063 - a035063

Published: Feb. 11, 2019

David L. Prole and Colin W. Taylor Department of Pharmacology, University Cambridge, Cambridge CB2 1PD, United Kingdom Correspondence: cwt1000{at}cam.ac.uk

Language: Английский

Reactive oxygen species (ROS) as pleiotropic physiological signalling agents DOI
Helmut Sies, Dean P. Jones

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(7), P. 363 - 383

Published: March 30, 2020

Language: Английский

Citations

3607

Defining roles of specific reactive oxygen species (ROS) in cell biology and physiology DOI
Helmut Sies, Vsevolod V. Belousov, Navdeep S. Chandel

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2022, Volume and Issue: 23(7), P. 499 - 515

Published: Feb. 21, 2022

Language: Английский

Citations

1034

Selective neuronal vulnerability in Parkinson disease DOI
D. James Surmeier, José Á. Obeso, Glenda M. Halliday

et al.

Nature reviews. Neuroscience, Journal Year: 2017, Volume and Issue: 18(2), P. 101 - 113

Published: Jan. 20, 2017

Language: Английский

Citations

909

Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: recent advances DOI Creative Commons
Wenzhang Wang, Fanpeng Zhao,

Xiaopin Ma

et al.

Molecular Neurodegeneration, Journal Year: 2020, Volume and Issue: 15(1)

Published: May 29, 2020

Abstract Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative diseases, characterized by impaired cognitive function due to progressive loss neurons in brain. Under microscope, neuronal accumulation abnormal tau proteins and amyloid plaques are two pathological hallmarks affected brain regions. Although detailed mechanism pathogenesis AD still elusive, a large body evidence suggests that damaged mitochondria likely play fundamental roles AD. It believed healthy pool not only supports activity providing enough energy supply other related mitochondrial functions neurons, but also guards minimizing oxidative damage. In this regard, exploration multitude mechanisms altered constitutes novel promising therapeutic targets for disease. review, we will summarize recent progress underscores essential role dysfunction discuss underlying with focus on structural functional integrity including biogenesis dynamics, axonal transport, ER-mitochondria interaction, mitophagy proteostasis.

Language: Английский

Citations

897

Redox metabolism: ROS as specific molecular regulators of cell signaling and function DOI

Claudia Lennicke,

Helena M. Cochemé

Molecular Cell, Journal Year: 2021, Volume and Issue: 81(18), P. 3691 - 3707

Published: Sept. 1, 2021

Language: Английский

Citations

690

The functional universe of membrane contact sites DOI
William A. Prinz,

Alexandre Toulmay,

Tamás Balla

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2019, Volume and Issue: 21(1), P. 7 - 24

Published: Nov. 15, 2019

Language: Английский

Citations

562

Mitochondrial dynamics in adaptive and maladaptive cellular stress responses DOI
Verónica Eisner, Martin Picard, György Hajnóczky

et al.

Nature Cell Biology, Journal Year: 2018, Volume and Issue: 20(7), P. 755 - 765

Published: June 22, 2018

Language: Английский

Citations

526

Microglia monitor and protect neuronal function through specialized somatic purinergic junctions DOI
Csaba Cserép, Balázs Pósfai, Nikolett Lénárt

et al.

Science, Journal Year: 2019, Volume and Issue: 367(6477), P. 528 - 537

Published: Dec. 13, 2019

Microglia are the main immune cells in brain and have roles homeostasis neurological diseases. Mechanisms underlying microglia-neuron communication remain elusive. Here, we identified an interaction site between neuronal cell bodies microglial processes mouse human brain. Somatic junctions a specialized nanoarchitecture optimized for purinergic signaling. Activity of mitochondria was linked with junction formation, which induced rapidly response to activation blocked by inhibition P2Y12 receptors. Brain injury-induced changes at somatic triggered receptor-dependent neuroprotection, regulating calcium load functional connectivity. Thus, these could potentially monitor protect functions.

Language: Английский

Citations

526

Calcium signalling in T cells DOI
Mohamed Trebak,

Jean-Pierre Kinet

Nature reviews. Immunology, Journal Year: 2019, Volume and Issue: 19(3), P. 154 - 169

Published: Jan. 8, 2019

Language: Английский

Citations

412

Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future DOI Creative Commons
Yun Zhang, Huaqiu Chen, Ran Li

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: June 30, 2023

Abstract Amyloid β protein (Aβ) is the main component of neuritic plaques in Alzheimer’s disease (AD), and its accumulation has been considered as molecular driver pathogenesis progression. Aβ prime target for development AD therapy. However, repeated failures Aβ-targeted clinical trials have cast considerable doubt on amyloid cascade hypothesis whether drug followed correct course. recent successes targeted assuaged those doubts. In this review, we discussed evolution over last 30 years summarized application diagnosis modification. particular, extensively pitfalls, promises important unanswered questions regarding current anti-Aβ therapy, well strategies further study more feasible approaches optimization prevention treatment.

Language: Английский

Citations

396