Reactive oxygen species (ROS) as pleiotropic physiological signalling agents

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(7), P. 363 - 383

Published: March 30, 2020

Language: Английский

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Molecular mechanisms of coronary microvascular endothelial dysfunction in diabetes mellitus: focus on mitochondrial quality surveillance

Angiogenesis, Journal Year: 2022, Volume and Issue: 25(3), P. 307 - 329

Published: March 18, 2022

Language: Английский

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Cisplatin-induced ototoxicity: From signaling network to therapeutic targets

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 157, P. 114045 - 114045

Published: Nov. 28, 2022

Administration of cisplatin, a common chemotherapeutic drug, has an inevitable side effect sensorineural hearing loss. The main etiologies are stria vascularis injury, spiral ganglion degeneration, and hair cell death. Over several decades, the research scope cisplatin-induced ototoxicity expanded with discovery molecular mechanism mediating inner ear death, highlighting roles reactive oxygen species transport channels for cisplatin uptake into cells. Upon entering cells, disrupts organelle metabolism, induces oxidative stress, targets DNA to cause intracellular damage. Recent studies have also reported role inflammation in ototoxicity. In this article, we preform narrative review latest mechanisms ototoxicity, from extracellular intracellular. We build up signaling network starting through blood labyrinth barrier, disrupting cochlear endolymph homeostasis, activating inflammatory responses outer After causes death via damage, redox system imbalance, mitochondrial endoplasmic reticulum dysfunction, culminating programmed including apoptosis, necroptosis, autophagic pyroptosis, ferroptosis. Based on mentioned mechanisms, prominent therapeutic targets, such as channel-blocking drugs transporter, construction structural analogues, anti-inflammatory drugs, antioxidants, inhibitors, others, were collated. Considering recent efforts, analyzed feasibility aforementioned strategies proposed our otoprotective approaches overcome

Language: Английский

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Nuclear genome-derived circular RNA circPUM1 localizes in mitochondria and regulates oxidative phosphorylation in esophageal squamous cell carcinoma

Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)

Published: Feb. 14, 2022

Abstract Circular RNAs (circRNAs) were shown to play an important role in the occurrence and progression of tumors. However, functions nuclear genome-derived circRNAs localized mitochondria tumor cells remain largely elusive. Here, we report that circPUM1, a circular RNA derived from back-splicing pre-mRNAs genome PUM1, localizes mitochondria. The expression level circPUM1 is positively correlated with HIF1α accumulation under CoCl 2 -induced intracellular hypoxic-like condition esophageal squamous cell carcinoma (ESCC) lines. Importantly, acts as scaffold for interaction between UQCRC1 UQCRC2 ESCC Knock-down would result lower oxygen concentration, downregulated oxidative phosphorylation, decrease mitochondrial membrane potential, increase ROS generation shrinking mitochondria, respectively. CircPUM1 depletion induces dysfunction complex III cleavage caspase3 spontaneously. Interestingly, disruption led pyroptosis initiates death Therefore, conclude plays critical maintaining stability enhance phosphorylation ATP production moreover propose exploit during adaptation.

Language: Английский

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Cellular rejuvenation: molecular mechanisms and potential therapeutic interventions for diseases

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: March 14, 2023

Abstract The ageing process is a systemic decline from cellular dysfunction to organ degeneration, with more predisposition deteriorated disorders. Rejuvenation refers giving aged cells or organisms youthful characteristics through various techniques, such as reprogramming and epigenetic regulation. great leaps in rejuvenation prove that not one-way street, many rejuvenative interventions have emerged delay even reverse the process. Defining mechanism by which roadblocks signaling inputs influence complex programs essential for understanding developing strategies. Here, we discuss intrinsic extrinsic factors counteract cell rejuvenation, targeted core mechanisms involved this Then, critically summarize latest advances state-of-art strategies of rejuvenation. Various methods also provide insights treating specific ageing-related diseases, including reprogramming, removal senescence (SCs) suppression senescence-associated secretory phenotype (SASP), metabolic manipulation, stem cells-associated therapy, dietary restriction, immune heterochronic transplantation, etc. potential applications therapy extend cancer treatment. Finally, analyze detail therapeutic opportunities challenges technology. Deciphering will further into anti-ageing disease treatment clinical settings.

Language: Английский

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Crosstalk between ferroptosis and cuproptosis: From mechanism to potential clinical application

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 171, P. 116115 - 116115

Published: Jan. 5, 2024

Ferroptosis and cuproptosis, regulated forms of cell death resulting from metal ion accumulation, are closely related in terms occurrence, metabolism, signaling pathways, drug resistance. Notably, it is now understood that these processes play crucial roles regulating physiological pathological processes, especially tumor development. Consequently, ferroptosis cuproptosis have gained increasing significance as potential targets for anti-cancer This article systematically outlines the molecular mechanisms cross-talk components both elucidating their impacts on cancer. Furthermore, investigates clinical perspective targeted cancer chemotherapy, immunotherapy, radiotherapy. Our discussion extends to a comparative analysis nanoparticles developed based cancer, contrasting them with current conventional therapies. Opportunities challenges treatment explored, emphasizing therapeutic direction co-targeting cuproptosis. The also attempts analyze applications this approach while summarizing existing barriers require overcoming.

Language: Английский

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Zishen Tongyang Huoxue decoction (TYHX) alleviates sinoatrial node cell ischemia/reperfusion injury by directing mitochondrial quality control via the VDAC1–β-tubulin signaling axis

Journal of Ethnopharmacology, Journal Year: 2023, Volume and Issue: 320, P. 117371 - 117371

Published: Nov. 18, 2023

Language: Английский

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Mitochondrial Structure and Function in Human Heart Failure

Circulation Research, Journal Year: 2024, Volume and Issue: 135(2), P. 372 - 396

Published: July 4, 2024

Despite clinical and scientific advancements, heart failure is the major cause of morbidity mortality worldwide. Both mitochondrial dysfunction inflammation contribute to development progression failure. Although crucial reparative healing following acute cardiomyocyte injury, chronic damages heart, impairs function, decreases cardiac output. Mitochondria, which comprise one third volume, may prove a potential therapeutic target for Known primarily energy production, mitochondria are also involved in other processes including calcium homeostasis regulation cellular apoptosis. Mitochondrial function closely related morphology, alters through dynamics, thus ensuring that needs cell met. However, failure, changes substrate use lead impaired myocyte function. This review discusses cristae role contact site organizing system complex ultrastructure changes. Additionally, this covers mitochondria-endoplasmic reticulum sites, communication via nanotunnels, altered metabolite production during We highlight these often-neglected factors promising targets

Language: Английский

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Aging, Cellular Senescence, and Glaucoma

Aging and Disease, Journal Year: 2024, Volume and Issue: 15(2), P. 546 - 546

Published: Jan. 1, 2024

Aging is one of the most serious risk factors for glaucoma, and according to age-standardized prevalence, glaucoma second leading cause legal blindness worldwide. Cellular senescence a hallmark aging that defined by stable exit from cell cycle in response cellular damage stress. The potential mechanisms underlying glaucomatous include oxidative stress, DNA damage, mitochondrial dysfunction, defective autophagy/mitophagy, epigenetic modifications. These phenotypes interact generate sufficiently network maintain senescent state. Senescent trabecular meshwork (TM) cells, retinal ganglion cells (RGCs) vascular endothelial reportedly accumulate with age stress may contribute pathologies. Therapies targeting suppression or elimination have been found ameliorate RGC death improve vision models, suggesting pivotal role pathophysiology glaucoma. In this review, we explore biological links between specifically delving into senescence. Moreover, summarize current data on key target associated development clinical Finally, discuss therapeutic management

Language: Английский

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Mitochondrial quality surveillance as a therapeutic target in myocardial infarction

Acta Physiologica, Journal Year: 2020, Volume and Issue: 231(3)

Published: Dec. 3, 2020

Abstract Myocardial infarction (MI) is a leading cause of morbidity and mortality worldwide. As mitochondrial dysfunction critically contributes to the pathogenesis MI, intensive research focused on development therapeutic strategies targeting homeostasis. Mitochondria possess quality control system which maintains restores their structure function by regulating fission, fusion, biogenesis, degradation death. In response slight damage such as transient hypoxia or mild oxidative stress, metabolism shifts from phosphorylation glycolysis, in order reduce oxygen consumption maintain ATP output. Mitochondrial dynamics are also activated modify shape structure, meet cardiomyocyte energy requirements through augmenting reducing mass. When damaged mitochondria cannot be repaired, poorly structured will degraded mitophagy, process often accompanied biogenesis. Once insult severe enough induce lethal cell, death pathway activation an inevitable consequence, apoptosis necrosis program initiated remove cells. surveillance hierarchical preserving defending cardiomyocytes against stress. A failure this has been regarded one potential pathologies underlying MI. review, we discuss recent findings focusing role highlight available approaches during

Language: Английский

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