The interplay of ROS and the PI3K/Akt pathway in autophagy regulation DOI

Lakhan Kma,

Taranga Jyoti Baruah

Biotechnology and Applied Biochemistry, Journal Year: 2021, Volume and Issue: 69(1), P. 248 - 264

Published: Jan. 15, 2021

Autophagy causes the breakdown of damaged proteins and organelles to their constituent components. The phosphatidylinositol 3-kinase (PI3K) pathway played an important role in regulating autophagic response cells changing reactive oxygen species (ROS) levels. PI3K α catalytic subunit inhibits autophagy, while its β promotes autophagy changes ROS downstream Akt protein acts against initiation increases levels under nutrient-rich conditions. by activating a mechanistic target rapamycin complex 1 (mTORC1) arresting gene expression. AMP-activated kinase (AMPK) counteracts actions. mTORC1 mTORC2 inhibit moderate levels, but high can promote cellular senescence via autophagy. Phosphatase tensin homolog (PTEN) are negative regulators pathway, it has proautophagic activities. Studies conducted on treated with flavonoids ionizing radiation showed that increase flavonoid-treated groups corresponded higher PTEN lowered leading occurrence In contrast, evoked caused lowering incidence

Language: Английский

Oxidative Stress DOI
Helmut Sies, Carsten Berndt, Dean P. Jones

et al.

Annual Review of Biochemistry, Journal Year: 2017, Volume and Issue: 86(1), P. 715 - 748

Published: April 25, 2017

Oxidative stress is two sided: Whereas excessive oxidant challenge causes damage to biomolecules, maintenance of a physiological level challenge, termed oxidative eustress, essential for governing life processes through redox signaling. Recent interest has focused on the intricate ways by which signaling integrates these converse properties. Redox balance maintained prevention, interception, and repair, concomitantly regulatory potential molecular thiol-driven master switches such as Nrf2/Keap1 or NF-κB/IκB used system-wide response. Nonradical species hydrogen peroxide (H2O2) singlet oxygen, rather than free-radical species, perform major second messenger functions. Chemokine-controlled NADPH oxidases metabolically controlled mitochondrial sources H2O2 well glutathione- thioredoxin-related pathways, with powerful enzymatic back-up systems, are responsible fine-tuning This makes rich research field spanning from biochemistry cell biology into nutritional sciences, environmental medicine, knowledge-based medicine.

Language: Английский

Citations

2756
Oxidative Stress in Cancer DOI Creative Commons
John D. Hayes, Albena T. Dinkova‐Kostova, Kenneth D. Tew

et al.

Cancer Cell, Journal Year: 2020, Volume and Issue: 38(2), P. 167 - 197

Published: July 9, 2020

Language: Английский

Citations

1839
The PI3K–AKT network at the interface of oncogenic signalling and cancer metabolism DOI
Gerta Hoxhaj, Brendan D. Manning

Nature reviews. Cancer, Journal Year: 2019, Volume and Issue: 20(2), P. 74 - 88

Published: Nov. 4, 2019

Language: Английский

Citations

1535
Insulin action and resistance in obesity and type 2 diabetes DOI
Michael Czech

Nature Medicine, Journal Year: 2017, Volume and Issue: 23(7), P. 804 - 814

Published: July 1, 2017

Language: Английский

Citations

1069
Defining roles of specific reactive oxygen species (ROS) in cell biology and physiology DOI
Helmut Sies, Vsevolod V. Belousov, Navdeep S. Chandel

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2022, Volume and Issue: 23(7), P. 499 - 515

Published: Feb. 21, 2022

Language: Английский

Citations

1012
ROS, Cell Senescence, and Novel Molecular Mechanisms in Aging and Age‐Related Diseases DOI Creative Commons
Pierpaola Davalli, Tijana Mitić, Andrea Caporali

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2016, Volume and Issue: 2016(1)

Published: Jan. 1, 2016

The aging process worsens the human body functions at multiple levels, thus causing its gradual decrease to resist stress, damage, and disease. Besides changes in gene expression metabolic control, rate has been associated with production of high levels Reactive Oxygen Species (ROS) and/or Nitrosative (RNS). Specific increases ROS level have demonstrated as potentially critical for induction maintenance cell senescence process. Causal connection between ROS, aging, age‐related pathologies, is studied intensely. Senescent cells proposed a target interventions delay related diseases or improve treatment. Therapeutic towards senescent might allow restoring health curing that share basal processes, rather than each disease separate symptomatic way. Here, we review observations on ability inducing through novel mechanisms underpin processes. Particular emphasis addressed involvement epigenetic regulation aim individuate specific pathways, which promote healthy lifespan aging.

Language: Английский

Citations

875
Molecular mechanisms of ROS production and oxidative stress in diabetes DOI Open Access
Philip Newsholme, Vinícius Fernandes Cruzat, Kevin N. Keane

et al.

Biochemical Journal, Journal Year: 2016, Volume and Issue: 473(24), P. 4527 - 4550

Published: Dec. 9, 2016

Oxidative stress and chronic inflammation are known to be associated with the development of metabolic diseases, including diabetes. stress, an imbalance between oxidative antioxidative systems cells tissues, is a result over production oxidative-free radicals reactive oxygen species (ROS). One outcome excessive levels ROS modification structure function cellular proteins lipids, leading dysfunction impaired energy metabolism, altered cell signalling cycle control, transport mechanisms overall dysfunctional biological activity, immune activation inflammation. Nutritional such as that caused by excess high-fat and/or carbohydrate diets, promotes evident increased lipid peroxidation products, protein carbonylation decreased antioxidant status. In obesity, underlying factors lead pathologies insulin resistance, dysregulated pathways diabetes cardiovascular disease through metabolism resulting in secretion, action responses. However, exercise may counter thus improve inflammatory outcomes. present article, we review molecular origins significance production, targets responses describing how affects secretion action, from point view possible application novel diabetic therapies based on redox regulation.

Language: Английский

Citations

761
Redox metabolism: ROS as specific molecular regulators of cell signaling and function DOI

Claudia Lennicke,

Helena M. Cochemé

Molecular Cell, Journal Year: 2021, Volume and Issue: 81(18), P. 3691 - 3707

Published: Sept. 1, 2021

Language: Английский

Citations

680
The Role of Sirtuins in Antioxidant and Redox Signaling DOI Open Access
Chandra K. Singh, Gagan Chhabra, Mary A. Ndiaye

et al.

Antioxidants and Redox Signaling, Journal Year: 2017, Volume and Issue: 28(8), P. 643 - 661

Published: Sept. 11, 2017

Antioxidant and redox signaling (ARS) events are regulated by critical molecules that modulate antioxidants, reactive oxygen species (ROS) or nitrogen (RNS), and/or oxidative stress within the cell. Imbalances in these can disturb cellular functions to become pathogenic. Sirtuins serve as important regulators of ARS cells. Recent Advances: (SIRTs 1-7) a family nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylases with ability deacetylate nonhistone targets. studies show sirtuins regulation variety processes associated ARS. SIRT1, SIRT3, SIRT5 protect cell from ROS, SIRT2, SIRT6, SIRT7 key genes mechanisms. Interestingly, SIRT4 has been shown induce ROS production antioxidative roles well.A complete understanding homeostasis is very understand normal functioning well pathological manifestations. In this review, we have provided discussion on role We also discussed mechanistic interactions among different sirtuins. Indeed, sirtuin biology could be at multiple fronts.Sirtuins emerging mammalian physiology stress-mediated situations. Studies needed dissect mechanisms maintaining homeostasis. Efforts required assess targetability management redox-regulated diseases. Antioxid. Redox Signal. 28, 643-661.

Language: Английский

Citations

672
ROS signaling under metabolic stress: cross-talk between AMPK and AKT pathway DOI Creative Commons
Zhao Yang, Xingbin Hu, Yajing Liu

et al.

Molecular Cancer, Journal Year: 2017, Volume and Issue: 16(1)

Published: April 13, 2017

Cancer cells are frequently confronted with metabolic stress in tumor microenvironments due to their rapid growth and limited nutrient supply. Metabolic induces cell death through ROS-induced apoptosis. However, cancer can adapt it by altering the pathways. AMPK AKT two primary effectors response stress: acts as an energy-sensing factor which rewires metabolism maintains redox balance. broadly promotes energy production abundance milieu, but role of under is dispute. Recent studies show that display antagonistic roles stress. stress-induced ROS signaling lies hub between reprogramming homeostasis. Here, we highlight cross-talk regulation on elimination, summarizes mechanism adaptability suggests potential options for therapeutics.

Language: Английский

Citations

595