Astaxanthin attenuates osteoarthritis progression via inhibiting ferroptosis and regulating mitochondrial function in chondrocytes

Wang, Xuezhong; Liu, Zilin; Peng, Puji; Gong, Ziheng; Huang, Jun; Peng, Hao

doi:10.1016/j.cbi.2022.110148

Cited by 61 publications

(29 citation statements)

References 65 publications

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“…A previous study reported that IL-6 could enhance the synthesis of FTH1 and FTL in hepatocytes ( Naz et al, 2013 ). It has been reported that inflammatory factors, such as IL-6 and IL-1β, have isozyme-specific effects on glutathione peroxidase (GPX) expression ( Shou et al, 2021 ; Wang et al, 2022 ). They increase GPX2 transcript concentration and decrease GPX4 transcript concentration.…”

Section: Discussionmentioning

confidence: 99%

Di-(2-ethylhexyl) phthalate exposure induces liver injury by promoting ferroptosis via downregulation of GPX4 in pregnant mice

Zhang

Zhen

Cheng

et al. 2022

Front. Cell Dev. Biol.

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As one kind of endocrine disrupting chemical, di-(2-ethylhexyl) phthalate (DEHP) has been reported to cause liver dysfunction in epidemiological and experimental studies. Abnormal liver function in pregnancy is associated with adverse maternal and perinatal outcomes. Few studies have investigated the potential effect of gestational DEHP exposure on the liver in pregnant mice, and the underlying mechanisms remain unclear. In the present study, pregnant ICR mice were exposed to doses (0, 500, 1,000 mg/kg/day) of DEHP in the presence or absence of 5 mg/kg/day ferrostatin-1 (Fer-1, ferroptosis inhibitor) by oral gavage from gestation day 4 to day 18. HepG2 cells were exposed to different doses of monoethylhexyl phthalate (MEHP, a major metabolite of DEHP) in vitro. Hepatic function and pathologic changes were observed. Oxidative stress, iron metabolism, and ferroptosis-related indicators and genes were evaluated both in vivo and in vitro. The results showed that gestational DEHP exposure induced disordered liver function and hepatocyte morphology changes in pregnant mice, along with increased malondialdehyde (MDA) and Fe2+ content and decreased glutathione (GSH) levels. The expression levels of the selected ferroptosis-related genes Slc7a11, Gpx4, and Nfr2 were significantly decreased, and Ptgs2 and Lpcat3 were significantly increased. Notably, Fer-1 attenuated DEHP-induced liver injury and ferroptosis. Furthermore, MEHP exhibited a synergistic effect with RSL3 (a GPX4 inhibitor) in promoting ferroptosis in vitro. Taken together, the results demonstrated that DEHP induced liver injury and ferroptosis in pregnant mice, probably by inhibiting the GPX4 pathway through lipid peroxidation and iron accumulation.

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Section: Discussionmentioning

confidence: 99%

Di-(2-ethylhexyl) phthalate exposure induces liver injury by promoting ferroptosis via downregulation of GPX4 in pregnant mice

Zhang

Zhen

Cheng

et al. 2022

Front. Cell Dev. Biol.

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“…Cysteine transport and glutathione synthesis is an important target of its development process. Ferroptosis can occur through a decrease in glutathione peroxidase 4 (GPX4) function [15], meanwhile can also be inhibited by inhibitors such as Fer-1. When the antioxidant capacity of cells goes down, ROS will accumulate in the cells and nally experience oxidative cellular death.…”

Section: Discussionmentioning

confidence: 99%

UAMC-3203 improves the inhibitory microenvironment to repair spinal cord injury by inhibiting ferroptosis

Kan

Zhao

Liu

et al. 2022

Preprint

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Background: Spinal cord injury (SCI) is a type of trauma to the nervous system that can lead to severe dysfunction of the motor and sensory systems. The inhibitory microenvironment is the basis of secondary injury after SCI, and ferroptosis may aggravate secondary SCI. In this study, the role of ferroptosis inhibitor UAMC-3203 in the recovery of SCI was explored by examining the tissue structure, biochemical indexes, and motor function of rats after SCI. Methods: A model of SCI was established using Alice's method. The protective effect of UAMC-3203 on spinal cord neurons and the recovery of motor function were studied by Basso, Beattie, Bresnahan (BBB) score, incline plate test, Hematoxylin-eosin (HE) staining and Luxol Fast Blue (LFB) staining. Immunofluorescence and Elisa analysis were used to study the effect of UAMC-3203 on the microenvironment. Western blot analysis was used to measure the level of ferroptosis markers. Reactive oxygen species (ROS) and malondialdehyde (MDA) were detected to reflect the level of oxidation products. Results: We found that in the UAMC-3203 group, the loss and demyelination of neurons was reduced, the activation and proliferation of astrocytes and microglia and the secretion of related inflammatory cytokines was restrained, and motor function recovery was faster and better compared with those in the SCI group. Conclusions: UAMC-3203 has played an active role in the recovery process of SCI, providing evidence that post-SCI microenvironment imbalances are associated with ferroptosis.

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“…Health experts forecast that by 2050, there will be a 310 % increase in hip fractures among elderly men and a 240 % increase among elderly women. Preventing and treating osteoporosis occurrence and progression is therefore a pressing matter in global health [56][57][58][59][60][61][62].…”

Section: Reported Connection Between Osteoporosis and Ferroptosismentioning

confidence: 99%

Ferroptosis: A Frontier in Osteoporosis

Maheshwari,

Singh,

Verma

2024

Horm Metab Res

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Reduced bone mass and degeneration of the microarchitecture of bone tissue are the hallmarks of osteoporosis, a bone metabolic disease that increases skeletal fragility and fracture susceptibility. Osteoporosis is primarily caused by unbalanced bone remodeling, in which bone synthesis is outpaced by bone resorption caused by osteoclasts. Along with the bone-building vitamins calcium and vitamin D, typical medications for treating osteoporosis include bisphosphonates and calcitonin. The present therapies effectively stop osteoclast activation that is too high, however they come with varying degrees of negative effects. Numerous factors can contribute to osteoporosis, which is characterized by a loss of bone mass and density due to the deterioration of the bone’s microstructure, which makes the bone more fragile. As a result, it is a systemic bone condition that makes patients more likely to fracture. Interest in the function of ferroptosis in the pathophysiology of osteoporosis is developing. In this review, we go through the shape of the cell, the fundamental mechanisms of ferroptosis, the relationship between osteoclasts and osteoblasts, the association between ferroptosis and diabetic osteoporosis, steroid-induced osteoporosis, and the relationship between ferroptosis and postmenopausal osteoporosis. The functions of ferroptosis and osteoporosis in cellular function, signaling cascades, pharmacological inhibition, and gene silencing have been better understood thanks to recent advances in biomedical research.

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Astaxanthin attenuates osteoarthritis progression via inhibiting ferroptosis and regulating mitochondrial function in chondrocytes

Cited by 61 publications

References 65 publications

Di-(2-ethylhexyl) phthalate exposure induces liver injury by promoting ferroptosis via downregulation of GPX4 in pregnant mice

Di-(2-ethylhexyl) phthalate exposure induces liver injury by promoting ferroptosis via downregulation of GPX4 in pregnant mice

UAMC-3203 improves the inhibitory microenvironment to repair spinal cord injury by inhibiting ferroptosis

Ferroptosis: A Frontier in Osteoporosis

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