Hallmarks of aging: An expanding universe

Cell, Journal Year: 2023, Volume and Issue: 186(2), P. 243 - 278

Published: Jan. 1, 2023

Language: Английский

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Autophagy in Human Health and Disease

New England Journal of Medicine, Journal Year: 2013, Volume and Issue: 368(7), P. 651 - 662

Published: Feb. 13, 2013

This review discusses the cellular process of autophagy ("self-eating"), which plays key roles in normal development immune system and adaptation to stress, as well a wide range disease states.

Language: Английский

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Autophagy and Aging

Cell, Journal Year: 2011, Volume and Issue: 146(5), P. 682 - 695

Published: Sept. 1, 2011

Language: Английский

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Mitochondria and the Autophagy–Inflammation–Cell Death Axis in Organismal Aging

Science, Journal Year: 2011, Volume and Issue: 333(6046), P. 1109 - 1112

Published: Aug. 25, 2011

Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, damage can trigger the permeabilization membranes initiate apoptosis necrosis. Moreover, have an important role pro-inflammatory signaling. Autophagic turnover cellular constituents, be it general specific for (mitophagy), eliminates dysfunctional damaged mitochondria, thus counteracting degeneration, dampening inflammation, preventing unwarranted cell loss. Decreased expression genes that regulate autophagy mitophagy cause diseases which deficient quality control results inflammation death populations. Thus, a combination dysfunction insufficient may contribute aging-associated pathologies.

Language: Английский

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Autophagy and apoptosis dysfunction in neurodegenerative disorders

Progress in Neurobiology, Journal Year: 2013, Volume and Issue: 112, P. 24 - 49

Published: Nov. 6, 2013

Autophagy and apoptosis are basic physiologic processes contributing to the maintenance of cellular homeostasis. encompasses pathways that target long-lived cytosolic proteins damaged organelles. It involves a sequential set events including double membrane formation, elongation, vesicle maturation finally delivery targeted materials lysosome. Apoptotic cell death is best described through its morphology. characterized by rounding, blebbing, cytoskeletal collapse, cytoplasmic condensation, fragmentation, nuclear pyknosis, chromatin condensation/fragmentation, formation membrane-enveloped apoptotic bodies, rapidly phagocytosed macrophages or neighboring cells. Neurodegenerative disorders becoming increasingly prevalent, especially in Western societies, with larger percentage members living an older age. They have be seen not only as health problem, but since they care-intensive, also carry significant economic burden. Deregulation autophagy plays pivotal role etiology and/or progress many these diseases. Herein, we briefly review latest findings indicate involvement neurodegenerative We provide brief introduction focusing on mitochondria lysosomes. then highlight pathophysiology common like Alzheimer's diseases, Parkinson's disease, Huntington's disease Amyotrophic lateral sclerosis. Then, describe functions brain homeostasis, context aforementioned disorders. Finally, discuss different ways modulation may employed for therapeutic intervention during

Language: Английский

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Neuronal Cell Death

Physiological Reviews, Journal Year: 2018, Volume and Issue: 98(2), P. 813 - 880

Published: Feb. 28, 2018

Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity adult neurons to proliferate or be replaced. The concept used simple as there were just two three types, so we had work out which type was involved in our particular pathology then block it. However, now know that are at least a dozen ways for die, blocking mechanism may not prevent from dying, non-neuronal cells also contribute neuronal death. We review here mechanisms by intrinsic extrinsic apoptosis, oncosis, necroptosis, parthanatos, ferroptosis, sarmoptosis, autophagic death, autosis, autolysis, paraptosis, pyroptosis, phagoptosis, mitochondrial permeability transition. next explore development, those induced axotomy, aberrant cell-cycle reentry, glutamate (excitoxicity oxytosis), loss connected neurons, aggregated proteins unfolded protein response, oxidants, inflammation, microglia. reassess forms occur stroke Alzheimer’s disease, most pathologies involving discuss why has been difficult pinpoint involved, if matters, molecular overlap interplay between subroutines, therapeutic implications these multiple overlapping

Language: Английский

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Mitophagy: mechanisms, pathophysiological roles, and analysis

Biological Chemistry, Journal Year: 2012, Volume and Issue: 393(7), P. 547 - 564

Published: July 1, 2012

Abstract Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper functions. Indeed, mitophagy has been recently proposed to play roles in terminal differentiation red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, ischemia or drug-induced tissue injury. Removal autophagy requires two steps: induction general priming selective autophagic recognition. Recent progress studies reveals mediated either by the Pink1-Parkin signaling pathway mitophagic receptors Nix Bnip3. In this review, we summarize our current knowledge on mechanisms mitophagy. We also discuss pathophysiological assays used monitor

Language: Английский

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Autophagy in healthy aging and disease

Nature Aging, Journal Year: 2021, Volume and Issue: 1(8), P. 634 - 650

Published: Aug. 12, 2021

Language: Английский

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REST and stress resistance in ageing and Alzheimer’s disease

Nature, Journal Year: 2014, Volume and Issue: 507(7493), P. 448 - 454

Published: March 19, 2014

Language: Английский

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Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases

Nature reviews. Neuroscience, Journal Year: 2018, Volume and Issue: 20(1), P. 19 - 33

Published: Nov. 22, 2018

Language: Английский

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