The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism

Nature reviews. Cancer, Год журнала: 2019, Номер 20(2), С. 74 - 88

Опубликована: Ноя. 4, 2019

Язык: Английский

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Exercise-induced oxidative stress: Friend or foe?

Journal of sport and health science/Journal of Sport and Health Science, Год журнала: 2020, Номер 9(5), С. 415 - 425

Опубликована: Май 4, 2020

The first report demonstrating that prolonged endurance exercise promotes oxidative stress in humans was published more than 4 decades ago. Since this discovery, many ensuing investigations have corroborated the fact muscular increases production of reactive oxygen species (ROS) and results numerous tissues including blood skeletal muscles. Although several may contribute to exercise-induced ROS production, it is predicted contractions stimulate active muscle fibers a primary source during exercise. This contraction-induced generation associated with (1) oxidant damage (e.g., increased protein oxidation lipid peroxidation), (2) accelerated fatigue, (3) activation biochemical signaling pathways adaptation contracting fibers. While our understanding has advanced rapidly last decades, questions remain about whether are beneficial or harmful health. review addresses issue by discussing site(s) detailing health consequences production.

Язык: Английский

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Nrf2 and Ferroptosis: A New Research Direction for Neurodegenerative Diseases

Frontiers in Neuroscience, Год журнала: 2020, Номер 14

Опубликована: Апрель 21, 2020

Ferroptosis is a kind of regulated cell death (RCD) caused by the redox state disorder intracellular microenvironment controlled glutathione peroxidase 4 (GPX4), which inhibited iron chelators and lipophilic antioxidants. In addition to classical regulatory mechanisms, new factors for ferroptosis have been discovered in recent years, such as P53 pathway, ATF3/4 Beclin 1 (BECN1) some non-coding RNA. closely related cancer treatment, neurodegenerative diseases, ischemia-reperfusion organ, neurotoxicity, other particular, field diseases treatment has aroused people's interest. The nuclear factor E2 2 (Nrf2/NFE2L2) proved play key role neurodegeneration disease regulation. promotes progression while expression Nrf2 its target genes (Ho-1, Nqo-1, Trx) declined with aging, therefore, there still insufficient evidence networks diseases. this review, we will provide brief overview well an emphasis on mechanism regulating ferroptosis. We also highlight during process investigate theoretical basis further research relationship between treatment.

Язык: Английский

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The multifaceted role of reactive oxygen species in tumorigenesis

Cellular and Molecular Life Sciences, Год журнала: 2020, Номер 77(22), С. 4459 - 4483

Опубликована: Май 1, 2020

Язык: Английский

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Sleep Loss Can Cause Death through Accumulation of Reactive Oxygen Species in the Gut

Cell, Год журнала: 2020, Номер 181(6), С. 1307 - 1328.e15

Опубликована: Июнь 1, 2020

Язык: Английский

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Nrf2–ARE signaling in cellular protection: Mechanism of action and the regulatory mechanisms

Journal of Cellular Physiology, Год журнала: 2019, Номер 235(4), С. 3119 - 3130

Опубликована: Сен. 23, 2019

Abstract Oxidative stress is the increase in cellular oxidant concentration comparison to antioxidant titer. Toxic insults and many other diseased conditions are mediated through formation of such condition. Once redox equilibrium disrupted, system functions bring back cell homeostasis state. The field players cytoprotective machinery xenobiotic‐metabolizing enzymes that transcriptionally controlled by upstream regulatory pathways like Nrf2–ARE pathway AhR–XRE pathway. importance Nrf2 lies fact it activated a variety compounds has wide range inducers including metals, organic toxicants so forth. present review article aims discuss role protection also intends illuminate mechanisms control itself. This can add our knowledge how reacts survives against stressed conditions.

Язык: Английский

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Nrf2/Keap1/ARE signaling: Towards specific regulation

Life Sciences, Год журнала: 2021, Номер 291, С. 120111 - 120111

Опубликована: Окт. 31, 2021

Язык: Английский

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The Keap1‐Nrf2 System: A Mediator between Oxidative Stress and Aging

Oxidative Medicine and Cellular Longevity, Год журнала: 2021, Номер 2021(1)

Опубликована: Янв. 1, 2021

Oxidative stress, a term that describes the imbalance between oxidants and antioxidants, leads to disruption of redox signals causes molecular damage. Increased oxidative stress from diverse sources has been implicated in most senescence‐related diseases aging itself. The Kelch‐like ECH‐associated protein 1‐ (Keap1‐) nuclear factor‐erythroid 2‐related factor 2 (Nrf2) system can be used monitor stress; Keap1‐Nrf2 is closely associated with controls transcription multiple antioxidant enzymes. Simultaneously, signaling also modulated by more complex regulatory network, including phosphoinositide 3‐kinase (PI3K)/protein kinase B (Akt), C, mitogen‐activated kinase. This review presents information on aging‐related mechanisms involving Keap1‐Nrf2. Furthermore, we highlight several major involved Nrf2 unbinding Keap1, cysteine modification Keap1 phosphorylation Nrf2, PI3K/Akt/glycogen synthase 3 β , sequestosome 1, Bach1 c ‐ Myc . Additionally, discuss direct interaction mammalian target rapamycin pathway. In summary, focus recent progress research aging, providing an empirical basis for development antiaging drugs.

Язык: Английский

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Ferroptosis is essential for diabetic cardiomyopathy and is prevented by sulforaphane via AMPK/NRF2 pathways

Acta Pharmaceutica Sinica B, Год журнала: 2021, Номер 12(2), С. 708 - 722

Опубликована: Окт. 19, 2021

Herein, we define the role of ferroptosis in pathogenesis diabetic cardiomyopathy (DCM) by examining expression key regulators mice with DCM and a new ex vivo model. Advanced glycation end-products (AGEs), an important pathogenic factor DCM, were found to induce engineered cardiac tissues (ECTs), as reflected through increased levels Ptgs2 lipid peroxides decreased ferritin SLC7A11 levels. Typical morphological changes cardiomyocytes observed using transmission electron microscopy. Inhibition ferrostatin-1 deferoxamine prevented AGE-induced ECT remodeling dysfunction. Ferroptosis was also evidenced heart type 2 DCM. liproxstatin-1 development diastolic dysfunction at 3 months after onset diabetes. Nuclear erythroid 2-related (NRF2) activated sulforaphane inhibited cell both AGE-treated ECTs hearts upregulating The protective effect on AMP-activated protein kinase (AMPK)-dependent. These findings suggest that plays essential DCM; prevents associated via AMPK-mediated NRF2 activation. This suggests feasible therapeutic approach clinically prevent

Язык: Английский

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Roles of Autophagy in Oxidative Stress

International Journal of Molecular Sciences, Год журнала: 2020, Номер 21(9), С. 3289 - 3289

Опубликована: Май 6, 2020

Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role autophagy crucial mediator has been clarified expanded the pathological response to redox signalling. major sensor Reactive oxygen species (ROS) are highly reactive molecules that generated by-products cellular metabolism, principally mitochondria. Mitochondrial ROS (mROS) beneficial detrimental cells depending on their concentration location. mROS function messengers intracellular signalling at physiologically low level, whereas excessive production causes oxidative damage constituents thus incurs death. Hence, balance autophagy-related adaptation death important comprehend signalling-related pathogenesis. In this review, we attempt provide an overview basic mechanism context pathology.

Язык: Английский

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