Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases

Huang, Ping; Chen, Guangwei; Jin, Weifeng; Mao, Kunjun; Wan, Haitong

doi:10.3390/ijms23137292

Cited by 64 publications

(37 citation statements)

References 183 publications

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“…For example, nutrient depletion often triggers increased rates of ferroptosis [ 59 ]. Parthanatos can be induced by DNA damage [ 63 ], and its rate is substantially elevated due to oxidative stress in the tumor microenvironment or by cancer treatment using alkylating agents [ 64 ]. Oncosis can frequently occur in cancers with the altered expression of ion channels and compromised ion gradient [ 65 ].…”

Section: Circulating Tumor Nucleic Acid Release Mechanismsmentioning

confidence: 99%

Circulating tumor nucleic acids: biology, release mechanisms, and clinical relevance

et al. 2023

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Background Despite advances in early detection and therapies, cancer is still one of the most common causes of death worldwide. Since each tumor is unique, there is a need to implement personalized care and develop robust tools for monitoring treatment response to assess drug efficacy and prevent disease relapse. Main body Recent developments in liquid biopsies have enabled real-time noninvasive monitoring of tumor burden through the detection of molecules shed by tumors in the blood. These molecules include circulating tumor nucleic acids (ctNAs), comprising cell-free DNA or RNA molecules passively and/or actively released from tumor cells. Often highlighted for their diagnostic, predictive, and prognostic potential, these biomarkers possess valuable information about tumor characteristics and evolution. While circulating tumor DNA (ctDNA) has been in the spotlight for the last decade, less is known about circulating tumor RNA (ctRNA). There are unanswered questions about why some tumors shed high amounts of ctNAs while others have undetectable levels. Also, there are gaps in our understanding of associations between tumor evolution and ctNA characteristics and shedding kinetics. In this review, we summarize current knowledge about ctNA biology and release mechanisms and put this information into the context of tumor evolution and clinical utility. Conclusions A deeper understanding of the biology of ctDNA and ctRNA may inform the use of liquid biopsies in personalized medicine to improve cancer patient outcomes.

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Section: Circulating Tumor Nucleic Acid Release Mechanismsmentioning

confidence: 99%

Circulating tumor nucleic acids: biology, release mechanisms, and clinical relevance

et al. 2023

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“…The complex translocates into the nucleus, where it triggers DNA degradation and cell death. Parthanatos underlies a wide spectrum of diseases, including those affecting the nervous system, such as AD, PD and stroke [41,42].…”

Section: Parthanatosmentioning

confidence: 99%

Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings

2023

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Reactive oxygen species (ROS) have been described to induce a broad range of redox-dependent signaling reactions in physiological conditions. Nevertheless, an excessive accumulation of ROS leads to oxidative stress, which was traditionally considered as detrimental for cells and organisms, due to the oxidative damage they cause to biomolecules. During ageing, elevated ROS levels result in the accumulation of damaged proteins, which may exhibit altered enzymatic function or physical properties (e.g., aggregation propensity). Emerging evidence also highlights the relationship between oxidative stress and age-related pathologies, such as protein misfolding-based neurodegenerative diseases (e.g., Parkinson’s (PD), Alzheimer’s (AD) and Huntington’s (HD) diseases). In this review we aim to introduce the role of oxidative stress in physiology and pathology and then focus on the state-of-the-art techniques available to detect and quantify ROS and oxidized proteins in live cells and in vivo, providing a guide to those aiming to characterize the role of oxidative stress in ageing and neurodegenerative diseases. Lastly, we discuss recently published data on the role of oxidative stress in neurological disorders.

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“…AIF then interacts with MIF and recruits MIF to the nucleus to cleave DNA, causing massive DNA breaks and eventually cell death [ 157 , 158 , 160 , 161 ]. Parthanatos is widely present in different diseases, including cardiovascular diseases, renal diseases, diabetes mellitus, cerebral ischemia, and neurodegenerative diseases [ 162 , 163 , 164 ]. Parthanatos has been extensively studied and confirmed in PD for more than two decades [ 19 , 165 , 166 ].…”

Section: Mechanisms Of Dna Damage-mediated Neurotoxicity In Pdmentioning

confidence: 99%

DNA Damage-Mediated Neurotoxicity in Parkinson’s Disease

Wang

et al. 2023

IJMS

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Parkinson’s disease (PD) is the second most common neurodegenerative disease around the world; however, its pathogenesis remains unclear so far. Recent advances have shown that DNA damage and repair deficiency play an important role in the pathophysiology of PD. There is growing evidence suggesting that DNA damage is involved in the propagation of cellular damage in PD, leading to neuropathology under different conditions. Here, we reviewed the current work on DNA damage repair in PD. First, we outlined the evidence and causes of DNA damage in PD. Second, we described the potential pathways by which DNA damage mediates neurotoxicity in PD and discussed the precise mechanisms that drive these processes by DNA damage. In addition, we looked ahead to the potential interventions targeting DNA damage and repair. Finally, based on the current status of research, key problems that need to be addressed in future research were proposed.

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Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases

Cited by 64 publications

References 183 publications

Circulating tumor nucleic acids: biology, release mechanisms, and clinical relevance

Circulating tumor nucleic acids: biology, release mechanisms, and clinical relevance

Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings

DNA Damage-Mediated Neurotoxicity in Parkinson’s Disease

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