The role of ferroptosis in chronic intermittent hypoxia-induced cognitive impairment

Liu, Zhili; Huang, Yinpei; Wang, Xin; He, Yuxin; Li, Juan; Li, Bing

doi:10.1007/s11325-022-02760-6

Cited by 5 publications

(6 citation statements)

References 28 publications

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“…There are many complicated reasons for manifesting AD phenotype, ranging from NFTs and amyloid plaques to hypoxia and glucose metabolism impairment. With hypoxia (73), lysosomal storage disorders (74), and impaired glucose metabolism (75) serving as the new markers of AD symptoms, research on AD neurodegeneration must shift to a non-conventional direction instead of solely focusing on amyloid accumulation. Hence, we put forth this study as an attempt to steer AD research toward congenital disorders with an inherent risk of neurodegeneration and help bring new perspectives by analyzing molecular commonalities among them.…”

Section: Discussionmentioning

confidence: 99%

A disease similarity approach identifies short-lived Niemann-Pick type C disease mice with accelerated brain aging as a novel mouse model for Alzheimer’s disease and aging research

Gujjala,

Klimek,

Abyadeh

et al. 2024

Preprint

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Since its first description in 1906 by Dr. Alois Alzheimer, Alzheimer's disease (AD) has been the most common type of dementia. Initially thought to be caused by age-associated accumulation of plaques, in recent years, research has increasingly associated AD with lysosomal storage and metabolic disorders, and the explanation of its pathogenesis has shifted from amyloid and tau accumulation to oxidative stress and impaired lipid and glucose metabolism aggravated by hypoxic conditions. However, the underlying mechanisms linking those cellular processes and conditions to disease progression have yet to be defined. Here, we applied a disease similarity approach to identify unknown molecular targets of AD by using transcriptomic data from congenital diseases known to increase AD risk, namely Down Syndrome, Niemann Pick Disease Type C (NPC), and Mucopolysaccharidoses I. We uncovered common pathways, hub genes, and miRNAs across in vitro and in vivo models of these diseases as potential molecular targets for neuroprotection and amelioration of AD pathology, many of which have never been associated with AD. We then investigated common molecular alterations in brain samples from an NPC disease mouse model by juxtaposing them with brain samples of both human and mouse models of AD. Detailed phenotypic and molecular analyses revealed NPCmut mouse as a novel, short-lived in vivo model of AD characterized by accelerated brain aging, concluding that NPCmut mouse model can serve as a potential short-lived in vivo model for AD research and for understanding molecular factors affecting brain aging. This research represents the first comprehensive approach to congenital disease association with neurodegeneration and a new perspective on AD research while highlighting shortcomings and lack of correlation in diverse in vitro models. Our findings provide a foundation for future animal and clinical studies and will lead to a better understanding of the molecular mechanisms underpinning the observed association between neurological congenital diseases and AD, thus has the potential to accelerate diagnostic and therapeutic applications against common types of dementia.

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Section: Discussionmentioning

confidence: 99%

A disease similarity approach identifies short-lived Niemann-Pick type C disease mice with accelerated brain aging as a novel mouse model for Alzheimer’s disease and aging research

Gujjala,

Klimek,

Abyadeh

et al. 2024

Preprint

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“…In addition to HIFs, NRF2, the master regulator of oxidative stress signaling, also plays an important role in hypoxia-induced ferroptosis. Many studies reported that NRF mediates the regulation of ferroptosis induced by hypoxia or H/R [ 124 , 125 , 128 , 138 ], while another group of studies reported that targeting NRF2 could inhibit hypoxia-or H/R-induced ferroptosis [ 149 , 160 , 161 , 162 , 163 , 164 , 165 , 166 ].…”

Section: Discussionmentioning

confidence: 99%

“…Ferroptosis can also be induced in normal cells under hypoxia conditions. It was reported that chronic intermittent hypoxia (CIH) induced ferroptosis in the hippocampus, lung, liver, and cardiomyocytes by downregulating NRF2 and GPX4, as well as upregulating ACSL4, leading to cognitive impairment and injury of brain, lung liver, and heart [ 122 , 123 , 124 , 125 ]. In the brain, hypoxic-ischemic induces ferroptosis with the increased TFRC expression, and decreased expression of SLC7A11, TRX-1, and GPX4 [ 126 , 127 , 128 ].…”

Section: The Mechanism and Regulation Of Ferroptosis Modulated By Hyp...mentioning

confidence: 99%

Ferroptosis Regulated by Hypoxia in Cells

Zheng

Liang

Zhang

2023

Cells

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Ferroptosis is an oxidative damage-related, iron-dependent regulated cell death with intracellular lipid peroxide accumulation, which is associated with many physiological and pathological processes. It exhibits unique features that are morphologically, biochemically, and immunologically distinct from other regulated cell death forms. Ferroptosis is regulated by iron metabolism, lipid metabolism, anti-oxidant defense systems, as well as various signal pathways. Hypoxia, which is found in a group of physiological and pathological conditions, can affect multiple cellular functions by activation of the hypoxia-inducible factor (HIF) signaling and other mechanisms. Emerging evidence demonstrated that hypoxia regulates ferroptosis in certain cell types and conditions. In this review, we summarize the basic mechanisms and regulations of ferroptosis and hypoxia, as well as the regulation of ferroptosis by hypoxia in physiological and pathological conditions, which may contribute to the numerous diseases therapies.

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“…OSA is considered an independent risk factor for recurrent stroke 118 . Its main pathophysiological feature is chronic intermittent hypoxia (CIH) 9 .…”

Section: Ferroptosis and Obstructive Sleep Apneamentioning

confidence: 99%

“…Ferroptosis is a new form of non-apoptotic cell death first proposed by Dixon in 2012, which is characterized by intracellular iron overload and excessive accumulation of lipid peroxides and reactive oxygen species (ROS), and its occurrence is related to the three major metabolic disorders of intracellular iron, amino acid, and lipid 2,3 . In recent years, more and more studies have shown that ferroptosis is not only involved in the development of AIS but also in the development of AIS risk factors such as atherosclerosis, atrial fibrillation, hypertension, diabetes mellitus, obstructive sleep apnea, and so on [4][5][6][7][8][9] . The use of ferroptosis inhibitors such as ferrostatin-1 and deferoxamine can not only prevent neuronal cell death and reduce secondary brain injury after stroke to improve the prognosis of patients but also slow the pathological progression of AIS risk factors 8,[10][11][12][13][14] , which suggests that regulating ferroptosis may become a new method for the prevention and treatment of AIS.…”

Section: Introductionmentioning

confidence: 99%

Role of ferroptosis in the occurrence and progression of acute ischemic stroke

Meng

Cheng

et al. 2023

Preprint

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Ferroptosis is a new non-apoptotic form of regulatory cell death, which is characterized by intracellular iron overload and excessive accumulation of lipid peroxides and reactive oxygen species (ROS). Ferroptosis is closely related to intracellular iron, amino acid, and lipid metabolism disorders. Ferroptosis is increasingly recognized as an important process mediating the pathogenesis and progression of acute ischemic stroke, and it can be involved in influencing acute ischemic stroke and acute ischemic stroke risk factors atherosclerosis, atrial fibrillation, hypertension, diabetes mellitus, and obstructive sleep apnea. Therefore, understanding the mechanisms of ferroptosis regulation in different diseases may have significant implications for the preventive treatment and improvement of prognosis in patients with acute ischemic stroke and patients with risk factors for acute ischemic stroke. This article reviews not only the specific important mechanisms of ferroptosis in the development of acute ischemic stroke, but also the relevant associations between risk factors for acute ischemic stroke and ferroptosis, and describes the current limitations and future directions of ferroptosis in the pathogenesis of acute ischemic stroke and its risk factors.

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The role of ferroptosis in chronic intermittent hypoxia-induced cognitive impairment

Cited by 5 publications

References 28 publications

A disease similarity approach identifies short-lived Niemann-Pick type C disease mice with accelerated brain aging as a novel mouse model for Alzheimer’s disease and aging research

A disease similarity approach identifies short-lived Niemann-Pick type C disease mice with accelerated brain aging as a novel mouse model for Alzheimer’s disease and aging research

Ferroptosis Regulated by Hypoxia in Cells

Role of ferroptosis in the occurrence and progression of acute ischemic stroke

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