FUNDC1 alleviates doxorubicin-induced cardiotoxicity by restoring mitochondrial-endoplasmic reticulum contacts and blocked autophagic flux DOI Creative Commons
Weibin He, Zhongchan Sun,

Guang Tong

et al.

Theranostics, Journal Year: 2024, Volume and Issue: 14(9), P. 3719 - 3738

Published: Jan. 1, 2024

Autophagy dysregulation is known to be a mechanism of doxorubicin (DOX)-induced cardiotoxicity (DIC). Mitochondrial-Endoplasmic Reticulum Contacts (MERCs) are where autophagy initiates and autophagosomes form. However, the role MERCs in DIC remains elusive. FUNDC1 tethering protein MERCs. We aim investigate effect DOX on cardiomyocytes explore whether it involved dysregulated DIC.

Language: Английский

ROS: Basic Concepts, Sources, Cellular Signaling, and its Implications in Aging Pathways DOI Creative Commons
Arthur José Pontes Oliveira de Almeida, Júlio César Pinheiro Lúcio de Oliveira,

Larisse Virgolino da Silva Pontes

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2022, Volume and Issue: 2022, P. 1 - 23

Published: Oct. 19, 2022

Reactive oxygen species (ROS) are bioproducts of cellular metabolism. There is a range molecules with oxidizing properties known as ROS. Despite those being implied negatively in aging and numerous diseases, their key role signaling evident. ROS control several biological processes such inflammation, proliferation, cell death. The redox underlying these events one characteristic the new generation scientists aimed at defining environment. potential, which includes balance sources antioxidant system, implies an important target for understanding cells’ fate derived from signaling. In this review, we summarized chemical, balance, signaling, implications aging.

Language: Английский

Citations

161

The Influence of Oxidative Stress on Thyroid Diseases DOI Creative Commons

Joanna Kochman,

Karolina Jakubczyk,

Piotr Bargiel

et al.

Antioxidants, Journal Year: 2021, Volume and Issue: 10(9), P. 1442 - 1442

Published: Sept. 10, 2021

Thyroid diseases, including neoplasms, autoimmune diseases and thyroid dysfunctions, are becoming a serious social problem with rapidly increasing prevalence. The latter is increasingly linked to oxidative stress. There many methods for determining the biomarkers of stress, making it possible evaluate profile in patients compared healthy population. This opens up new perspective investigating role elevated parameters stress damage people especially neoplastic nature. An imbalance between oxidants antioxidants observed at different stages types diseases. organ, which part endocrine system, uses free radicals (reactive oxygen species, ROS) produce hormones. cells release enzymes that catalyse ROS generation; therefore, key played by internal defence system non-enzymatic counteract excess not utilised hormones, acting as buffer neutralise ensure whole-body homeostasis. causes structural cell damage, undermining genomic stability. Looking negative effects accumulation, appears be implicated both initiation progression carcinogenesis. aim this review investigate oxidation background summarise links redox dysfunction disease.

Language: Английский

Citations

121

Mitochondria as an important target of metformin: The mechanism of action, toxic and side effects, and new therapeutic applications DOI

Jin Feng,

Xiaohui Wang, Xiaochun Ye

et al.

Pharmacological Research, Journal Year: 2022, Volume and Issue: 177, P. 106114 - 106114

Published: Feb. 3, 2022

Language: Английский

Citations

102

Autophagy in Bone Remodeling: A Regulator of Oxidative Stress DOI Creative Commons

Chenyu Zhu,

Shiwei Shen, Shihua Zhang

et al.

Frontiers in Endocrinology, Journal Year: 2022, Volume and Issue: 13

Published: June 30, 2022

Bone homeostasis involves bone formation and resorption, which are processes that maintain skeletal health. Oxidative stress is an independent risk factor, causing the dysfunction of including osteoblast-induced osteogenesis osteoclast-induced osteoclastogenesis, thereby leading to bone-related diseases, especially osteoporosis. Autophagy main cellular response system for limination damaged organelles proteins, it plays a critical role in differentiation, apoptosis, survival cells, marrow stem cells (BMSCs), osteoblasts, osteoclasts, osteocytes. High evels reactive oxygen species (ROS) induced by oxidative induce autophagy protect against cell damage or even apoptosis. Additionally, pathways such as ROS/FOXO3, ROS/AMPK, ROS/Akt/mTOR, ROS/JNK/c-Jun involved regulation stress-induced osteocytes osteoclasts. This review discusses how regulates resorption following summarizes potential protective mechanisms exerted autophagy, providing new insights regarding remodeling therapeutic targets

Language: Английский

Citations

95

Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy DOI Creative Commons
Xiaoqing Liu, Riaz Hussain, Khalid Mehmood

et al.

BioMed Research International, Journal Year: 2022, Volume and Issue: 2022, P. 1 - 12

Published: Sept. 17, 2022

Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of (oxygen-containing molecules) ultimately leading to oxidative damage in terms lipid peroxidation, protein denaturation, DNA mutation. can activate autophagy alleviate maintain normal physiological activities cells by degrading damaged organelles or local cytoplasm. When not eliminated autophagy, it activates apoptosis cascade. This review provides a brief summary mitochondrial-endoplasmic reticulum communication-mediated autophagy. Mitochondria endoplasmic being important are directly indirectly connected each other through mitochondria-associated membranes jointly regulate The reactive oxygen species (ROS) produced mitochondrial respiratory chain main inducers stress. Damaged mitochondria be effectively cleared process mitophagy mediated PINK1/parkin pathway, Nix/BNIP3 pathways, FUNDC1 avoiding excessive ROS production. However, mechanism communication regulation rarely known. For this reason, explores mutual connection mediating Ca

Language: Английский

Citations

74

Unfolding the Interactions between Endoplasmic Reticulum Stress and Oxidative Stress DOI Creative Commons

Gideon Ong,

Susan E. Logue

Antioxidants, Journal Year: 2023, Volume and Issue: 12(5), P. 981 - 981

Published: April 22, 2023

Oxidative stress is caused by an imbalance in cellular redox state due to the accumulation of reactive oxygen species (ROS). While homeostatic levels ROS are important for cell physiology and signaling, excess can induce a variety negative effects ranging from damage biological macromolecules death. Additionally, oxidative disrupt function redox-sensitive organelles including mitochondria endoplasmic reticulum (ER). In case ER, misfolded proteins arise stress, leading onset ER stress. To combat cells initiate highly conserved response called unfolded protein (UPR). UPR within context resolving well characterised, how mediators respond influence less defined. this review, we evaluate interplay between signaling networks. Specifically, assess antioxidant responses.

Language: Английский

Citations

73

Roles of Oxidative Stress in Synaptic Dysfunction and Neuronal Cell Death in Alzheimer’s Disease DOI Creative Commons
Germán Plascencia‐Villa, George Perry

Antioxidants, Journal Year: 2023, Volume and Issue: 12(8), P. 1628 - 1628

Published: Aug. 17, 2023

Alzheimer’s disease (AD) is a brain disorder that progressively undermines memory and thinking skills by affecting the hippocampus entorhinal cortex. The main histopathological hallmarks of AD are presence abnormal protein aggregates (Aβ tau), synaptic dysfunction, aberrant proteostasis, cytoskeletal abnormalities, altered energy homeostasis, DNA RNA defects, inflammation, neuronal cell death. However, oxidative stress or damage also evident commonly overlooked considered consequence advancement dementia symptoms. control onset linked to activity amyloid-β peptide, which may serve as both antioxidant pro-oxidant molecules. Furthermore, correlated with proteins, nucleic acids, lipids in vulnerable populations, ultimately lead death through different molecular mechanisms. By recognizing an integral feature AD, alternative therapeutic preventive interventions developed tested potential complementary therapies for this devastating neurodegenerative disease.

Language: Английский

Citations

58

Mechanisms of and Potential Medications for Oxidative Stress in Ovarian Granulosa Cells: A Review DOI Open Access

Siheng Liu,

Yunbing Jia,

Shirui Meng

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(11), P. 9205 - 9205

Published: May 24, 2023

Granulosa cells are essential for follicle initiation and development, their abnormal function or apoptosis is a crucial factor leading to follicular atresia. A state of oxidative stress occurs when the balance between production reactive oxygen species regulation antioxidant system disturbed. Oxidative one most important causes granulosa cells. in female reproductive diseases, such as polycystic ovary syndrome premature ovarian failure. In recent years, studies have confirmed that mechanism closely linked PI3K-AKT signaling pathway, MAPK FOXO axis, Nrf2 NF-κB mitophagy. It has been found drugs sulforaphane, Periplaneta americana peptide, resveratrol can mitigate functional damage caused by on This paper reviews some mechanisms involved describes underlying pharmacological treatment

Language: Английский

Citations

50

Insights and implications of sexual dimorphism in osteoporosis DOI Creative Commons
Yuanyuan Zhang, Na Xie,

Xiaodong Sun

et al.

Bone Research, Journal Year: 2024, Volume and Issue: 12(1)

Published: Feb. 18, 2024

Osteoporosis, a metabolic bone disease characterized by low mineral density and deterioration of microarchitecture, has led to high risk fatal osteoporotic fractures worldwide. Accumulating evidence revealed that sexual dimorphism is notable feature osteoporosis, with sex-specific differences in epidemiology pathogenesis. Specifically, females are more susceptible than males while prone disability or death from the disease. To date, sex chromosome abnormalities steroid hormones have been proven contribute greatly osteoporosis regulating functions cells. Understanding its related complications essential for improving treatment strategies tailored women men. This literature review focuses on mechanisms underlying mainly population aging patients, chronic glucocorticoid administration, diabetes. Moreover, we highlight implications developing therapeutics preventive screening approaches Additionally, challenges translating bench research bedside treatments future directions overcome these obstacles will be discussed.

Language: Английский

Citations

30

Autophagy in aging-related diseases and cancer: Principles, regulatory mechanisms and therapeutic potential DOI
Na Wu, Wenhui Zheng,

Yundong Zhou

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 100, P. 102428 - 102428

Published: July 20, 2024

Language: Английский

Citations

22