Erratum to: From cell senescence to age-related diseases: differential mechanisms of action of senescence-associated secretory phenotypes

Byun, Hae‐Ok; Lee, Young-Kyoung; Kim, Jeong‐Min; Yoon, Gyesoon

doi:10.5483/bmbrep.2016.49.11.122

Cited by 33 publications

(3 citation statements)

References 99 publications

(106 reference statements)

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“…Age-associated chronic inflammation has also been attributed to the accumulation of senescent cells with a pro-inflammatory secretory phenotype [162]. Induced expression of miR-146a in human umbilical and coronary endothelium during replicative senescence indicates that TLR/NF-κB activation and cell senescence can be modulated by miR-146a [163].…”

Section: Mirs Involved In Telomere Shortening Cellular Senescencementioning

confidence: 99%

MicroRNAs and the Genetic Nexus of Brain Aging, Neuroinflammation, Neurodegeneration, and Brain Trauma

Sarkar¹,

Russell²,

Engler-Chiurazzi³

et al. 2019

Aging and disease

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Aging is a complex and integrated gradual deterioration of cellular activities in specific organs of the body, which is associated with increased mortality. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, neurovascular disorders, and neurodegenerative diseases. There are nine tentative hallmarks of aging. In addition, several of these hallmarks are increasingly being associated with acute brain injury conditions. In this review, we consider the genes and their functional pathways involved in brain aging as a means of developing new strategies for therapies targeted to the neuropathological processes themselves, but also as targets for many age-related brain diseases. A single microRNA (miR), which is a short, non-coding RNA species, has the potential for targeting many genes simultaneously and, like practically all other cellular processes, genes associated with many features of brain aging and injury are regulated by miRs. We highlight how certain miRs can mediate deregulation of genes involved in neuroinflammation, acute neuronal injury and chronic neurodegenerative diseases. Finally, we review the recent progress in the development of effective strategies to block specific miR functions and discuss future approaches with the prediction that anti-miR drugs may soon be used in the clinic.

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Section: Mirs Involved In Telomere Shortening Cellular Senescencementioning

confidence: 99%

MicroRNAs and the Genetic Nexus of Brain Aging, Neuroinflammation, Neurodegeneration, and Brain Trauma

Sarkar¹,

Russell²,

Engler-Chiurazzi³

et al. 2019

Aging and disease

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“…Cellular senescence, a state of permanent and irreversible cell-cycle arrest [ 62 ], is intimately linked to CVDs and was found in sick cardiovascular tissues [ 63 ]. Excessive arginase activity has been associated with EC senescence in aging humans and animals [ 64 ], and lowering arginase protein expression/activity reverses endothelial senescence [ 65 , 66 ].…”

Section: Arginase Mediates Various Cellular Functionsmentioning

confidence: 99%

Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases

Wang

Ren

et al. 2022

Cell Death Discov.

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Arginase, a binuclear manganese metalloenzyme in the urea, catalyzes the hydrolysis of L-arginine to urea and L-ornithine. Both isoforms, arginase 1 and arginase 2 perform significant roles in the regulation of cellular functions in cardiovascular system, such as senescence, apoptosis, proliferation, inflammation, and autophagy, via a variety of mechanisms, including regulating L-arginine metabolism and activating multiple signal pathways. Furthermore, abnormal arginase activity contributes to the initiation and progression of a variety of CVDs. Therefore, targeting arginase may be a novel and promising approach for CVDs treatment. In this review, we give a comprehensive overview of the physiological and biological roles of arginase in a variety of CVDs, revealing the underlying mechanisms of arginase mediating vascular and cardiac function, as well as shedding light on the novel and promising therapeutic approaches for CVDs therapy in individuals.

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“…Such an arrest is triggered by many stress factors including oxidative stress, telomere shortening, oncogenic activation, therapeutic toxicity, and mitochondrial stress [ 8 - 10 ]. Senescent cells have been shown to accumulate in aged tissue [ 8 , 10 ], and to be associated with a variety of age-related disorders including pulmonary and renal fibrosis, atherosclerosis, hepatic steatosis, hypertension, and lung, breast, and colorectal cancer [ 11 - 15 ]. In addition, dysfunctional senescent cells have been associated with several mitochondrial defects including increased mass, respiratory chain defects, OS, mitochondrial DNA (mtDNA) mutations, and structural abnormalities [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Comprehensive investigations of key mitochondrial metabolic changes in senescent human fibroblasts

Ghneim

Alfhili

Alharbi

et al. 2022

Korean J Physiol Pharmacol

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There is a paucity of detailed data related to the effect of senescence on the mitochondrial antioxidant capacity and redox state of senescent human cells. Activities of TCA cycle enzymes, respiratory chain complexes, hydrogen peroxide (H 2 O 2 ), superoxide anions (SA), lipid peroxides (LPO), protein carbonyl content (PCC), thioredoxin reductase 2 (TrxR2), superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPx1), glutathione reductase (GR), reduced glutathione (GSH), and oxidized glutathione (GSSG), along with levels of nicotinamide cofactors and ATP content were measured in young and senescent human foreskin fibroblasts. Primary and senescent cultures were biochemically identified by monitoring the augmented cellular activities of key glycolytic enzymes including phosphofructokinase, lactate dehydrogenase, and glycogen phosphorylase, and accumulation of H 2 O 2 , SA, LPO, PCC, and GSSG. Citrate synthase, aconitase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, and complex I-III, II-III, and IV activities were significantly diminished in P25 and P35 cells compared to P5 cells. This was accompanied by significant accumulation of mitochondrial H 2 O 2 , SA, LPO, and PCC, along with increased transcriptional and enzymatic activities of TrxR2, SOD2, GPx1, and GR. Notably, the GSH/GSSG ratio was significantly reduced whereas NAD + /NADH and NADP + /NADPH ratios were significantly elevated. Metabolic exhaustion was also evident in senescent cells underscored by the severely diminished ATP/ADP ratio. Profound oxidative stress may contribute, at least in part, to senescence pointing at a potential protective role of antioxidants in aging-associated disease.

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Erratum to: From cell senescence to age-related diseases: differential mechanisms of action of senescence-associated secretory phenotypes

Cited by 33 publications

References 99 publications

MicroRNAs and the Genetic Nexus of Brain Aging, Neuroinflammation, Neurodegeneration, and Brain Trauma

MicroRNAs and the Genetic Nexus of Brain Aging, Neuroinflammation, Neurodegeneration, and Brain Trauma

Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases

Comprehensive investigations of key mitochondrial metabolic changes in senescent human fibroblasts

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