Redox changes and cellular senescence in Alzheimer's disease

Yu, Nicole; Pasha, Mazhar; Chua, John Jia En

doi:10.1016/j.redox.2024.103048

Cited by 6 publications

(2 citation statements)

References 158 publications

(170 reference statements)

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“…The imbalance between oxidative and antioxidant systems can instigate the onset and progression of various diseases such as heart failure [ 53 ] and Alzheimer’s disease [ 54 ], while also causing significant damage to organs and tissues. Oxidative stress triggers the release of reactive oxygen species (ROS), activating diverse signaling pathways and influencing gene and protein expression.…”

Section: Protective Effects and Action Mechanisms Of Asmentioning

confidence: 99%

Artesunate Exerts Organ- and Tissue-Protective Effects by Regulating Oxidative Stress, Inflammation, Autophagy, Apoptosis, and Fibrosis: A Review of Evidence and Mechanisms

Zhu,

Wang,

Han

et al. 2024

Antioxidants

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The human body comprises numerous organs and tissues operating in synchrony, it facilitates metabolism, circulation, and overall organismal function. Consequently, the well-being of our organs and tissues significantly influences our overall health. In recent years, research on the protective effects of artesunate (AS) on various organ functions, including the heart, liver, brain, lungs, kidneys, gastrointestinal tract, bones, and others has witnessed significant advancements. Findings from in vivo and in vitro studies suggest that AS may emerge as a newfound guardian against organ damage. Its protective mechanisms primarily entail the inhibition of inflammatory factors and affect anti-fibrotic, anti-aging, immune-enhancing, modulation of stem cells, apoptosis, metabolic homeostasis, and autophagy properties. Moreover, AS is attracting a high level of interest because of its obvious antioxidant activities, including the activation of Nrf2 and HO-1 signaling pathways, inhibiting the release of reactive oxygen species, and interfering with the expression of genes and proteins associated with oxidative stress. This review comprehensively outlines the recent strides made by AS in alleviating organismal injuries stemming from various causes and protecting organs, aiming to serve as a reference for further in-depth research and utilization of AS.

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Section: Protective Effects and Action Mechanisms Of Asmentioning

confidence: 99%

Artesunate Exerts Organ- and Tissue-Protective Effects by Regulating Oxidative Stress, Inflammation, Autophagy, Apoptosis, and Fibrosis: A Review of Evidence and Mechanisms

Zhu,

Wang,

Han

et al. 2024

Antioxidants

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“…21 For years, we've acknowledged the crucial role of mitochondrial impairment in inducing cellular senescence and ageing progression. 22 Recent findings suggest that malfunctioning or damaged mitochondria escalate cellular senescence via amplified reactive oxygen species (ROS) production. This can occur through compromised electron transfer in the electron transport chain (ETC), resulting in elevated ROS generation.…”

Section: Mitochondrial Oxidative Stressmentioning

confidence: 99%

Infectious viruses and neurodegenerative diseases: The mitochondrial defect hypothesis

Jiang,

Zhu,

Kang

et al. 2024

Reviews in Medical Virology

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Global attention is riveted on neurodegenerative diseases due to their unresolved aetiologies and lack of efficacious therapies. Two key factors implicated include mitochondrial impairment and microglial ageing. Several viral infections, including Herpes simplex virus‐1 (HSV‐1), human immunodeficiency virus (HIV) and Epstein‐Barr virus, are linked to heightened risk of these disorders. Surprisingly, numerous studies indicate viruses induce these aforementioned precipitating events. Epstein‐Barr virus, Hepatitis C Virus, HIV, respiratory syncytial virus, HSV‐1, Japanese Encephalitis Virus, Zika virus and Enterovirus 71 specifically impact mitochondrial function, leading to mitochondrial malfunction. These vital organelles govern various cell activities and, under specific circumstances, trigger microglial ageing. This article explores the role of viral infections in elucidating the pathogenesis of neurodegenerative ailments. Various viruses instigate microglial ageing via mitochondrial destruction, causing senescent microglia to exhibit activated behaviour, thereby inducing neuroinflammation and contributing to neurodegeneration.

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Trending toward gero‐electroceuticals that target membrane potential for reprogramming aging and lifespan

Tabibzadeh,

Brown

2024

Aging and Cancer

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Ion gradients across cell membranes generate voltage potentials that are involved in a wide range of biological processes. According to the membrane hypothesis of aging, aging is inextricably linked to a decrease in resting membrane potential (Vmem). Alterations in ion channel activity and membrane fluidity caused by aging disrupt bioelectric homeostasis, increase intracellular calcium and potassium concentrations, induce abnormal mechanistic target of rapamycin (MTOR)‐ and AMPK‐regulated metabolism and energy dissipation, and decrease proliferation and regeneration. Failure to maintain ion channel activity and membrane potential leads to cell senescence or death. There is evidence that by manipulating ion channel activities, a cryptic memory can be recalled to restore lost proliferative or regenerative abilities. Reversal or prevention of senescence, aging phenotypes, and longevity may be achieved by fine‐tuning mitochondrial membrane polarization. Therefore, there is optimism that deciphering the bioelectric codes that govern cell functions will lead to the development of new gero‐electroceuticals that restore cell function and prevent tissue loss during aging.

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Redox changes and cellular senescence in Alzheimer's disease

Cited by 6 publications

References 158 publications

Artesunate Exerts Organ- and Tissue-Protective Effects by Regulating Oxidative Stress, Inflammation, Autophagy, Apoptosis, and Fibrosis: A Review of Evidence and Mechanisms

Artesunate Exerts Organ- and Tissue-Protective Effects by Regulating Oxidative Stress, Inflammation, Autophagy, Apoptosis, and Fibrosis: A Review of Evidence and Mechanisms

Infectious viruses and neurodegenerative diseases: The mitochondrial defect hypothesis

Trending toward gero‐electroceuticals that target membrane potential for reprogramming aging and lifespan

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