Inhibition of the NADPH Oxidase Pathway Reduces Ferroptosis during Septic Renal Injury in Diabetic Mice

Yao, Weifeng; Liao, Haofeng; Pang, Mengya; Pan, Longfa; Guan, Yu; Huang, Xiaolei; Hei, Ziqing; Luo, Chenfang; Ge, Mian

doi:10.1155/2022/1193734

Cited by 32 publications

(14 citation statements)

References 33 publications

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“…Fang et al [ 36 ] showed that ferroptosis could enhance autophagy by inhibiting PI3K, downregulate the expression of beclin-1, upregulate the expression of p62, and reduce the ratio of LC3 II/LC3 I, thus reducing the inflammatory response of macrophages induced by LPS. After neuronal apoptosis, ferroptosis treatment can significantly downregulate the mRNA and protein expression levels of beclin-1 and LC3 II/lc3 I, inhibit autophagy, and play an organ protective role [ 37 ]. Under normal circumstances, the autophagy level of the body is low.…”

Section: Effect Of Ferroptosis On Anti-inflammatory Activity Of Macro...mentioning

confidence: 99%

Ferroptosis in Macrophage Impairment in Sepsis

Liu

2022

Applied Bionics and Biomechanics

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Sepsis is a clinical syndrome with high mortality, which can lead to multiple organ dysfunction syndrome. Nonspecific immune dysfunction and immune imbalance are its important pathological features. Macrophages are important immune cells and one of the important components of innate and adaptive immunity. Regulating the function of macrophages may be a potential method for the treatment of sepsis. Up to now, ferroptosis has been proved to be involved in the pathophysiological mechanism of many diseases, such as Alzheimer’s disease, cancer, Parkinson’s disease, and renal degeneration. At present, relevant studies have reported that ferroptosis may be involved in the occurrence of sepsis This paper reviews the existing mechanisms of iron ptosis in macrophages in sepsis, with a view to providing si’l for future studies on sepsis.

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Section: Effect Of Ferroptosis On Anti-inflammatory Activity Of Macro...mentioning

confidence: 99%

Ferroptosis in Macrophage Impairment in Sepsis

Liu

2022

Applied Bionics and Biomechanics

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“…The early phase of HTGP is generally believed to be an unregulated inflammatory response or a cytokine storm that results in organ damage and death[ 31 , 32 ]. Pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, are considered pivotal mediators for initiating, amplifying, and perpetuating organ injury[ 33 - 35 ].…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis inhibition attenuates inflammatory response in mice with acute hypertriglyceridemic pancreatitis

Meng¹,

Zhou²,

Han³

et al. 2023

World J Gastroenterol

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BACKGROUND Ferroptosis is involved in developing inﬂammatory diseases; yet, its role in acute hypertriglyceridemic pancreatitis (HTGP) remains unclear. AIM To explore whether ferroptosis is involved in the process of HTGP and elucidate its potential mechanisms. METHODS An HTGP mouse model was induced using intraperitoneal injection of P-407 and caerulein (CAE). Then, pancreatic tissues from the model animals were subjected to proteome sequencing analysis. The pathological changes and scores of the pancreas, lung, and kidney were determined using hematoxylin-eosin staining. The levels of serum amylase (AMY), triglyceride, and total cholesterol were measured with an automatic blood cell analyzer. Additionally, the serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β were determined by enzyme linked immunosorbent assay. Malonaldehyde (MDA), glutathione (GSH), and Fe 2+ were detected in the pancreas. Finally, immunohistochemistry was performed to assess the expression of ferroptosis-related proteins. RESULTS Proteome sequencing revealed that ferroptosis was involved in the process of HTGP and that NADPH oxidase (NOX) 2 may participate in ferroptosis regulation. Moreover, the levels of serum AMY, TNF-α, IL-6, and IL-1β were significantly increased, MDA and Fe 2+ were upregulated, GSH and ferroptosis-related proteins were reduced, and the injury of the pancreas, lung, and kidney were aggravated in the P407 + CAE group compared to CAE and wild type groups (all P < 0.05). Notably, the inhibition of ferroptosis and NOX2 attenuated the pathological damage and the release of TNF-α, IL-6, and IL-1β in the serum of the mice. CONCLUSION Ferroptosis was found to have an important role in HTGP and may be considered a potential target for clinical treatment.

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“…In our study, we found that Fer‐1 and DFO can effectively support bone regeneration through increasing the abundance of type H vessels and osteoprogenitors. Moreover, Fer‐1 and DFO have proven effective to treat obesity‐related liver and kidney diseases 38,84–86 . Therefore, Fer‐1 and DFO are potential drugs for the treatment of obesity‐related osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

Interaction between ferroptosis and TNF‐α: Impact in obesity‐related osteoporosis

Chen

Liu

et al. 2023

The FASEB Journal

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The relationship of obesity and osteoporosis has been widely studied over the past years. However, the implications of obesity for bone health remain controversial, and the underlying molecular mechanism is not yet fully understood.This study demonstrated that high-fat diet-induced obesity leads to significantly decreased bone volume/tissue volume (BV/TV), trabecular number (Tb.N), and cortical thickness (Ct.Th) of male rat femur after mechanical loading effects of body weight were controlled. HFD-induced obese rats exhibited attenuated expression of ferroptosis inhibitory protein SLC7A11 and GPX4 in bone tissues, which was correlated with elevated serum TNF-α concentration. Ferroptosis inhibitor administration could effectively rescue decreased osteogenesis-associated type H vessels and osteoprogenitors, and downregulate serum levels of TNF-α to ameliorate bone loss in obese rats. Since ferroptosis and TNF-α both affect bone and vessel formation, we further investigated the interaction between ferroptosis and TNF-α, and its impact in osteogenesis and angiogenesis in vitro. In human osteoblast-like MG63 and umbilical vein endothelial cells (HUVEC), TNF-α/ TNFR2 signaling promoted cystine uptake and GSH biosynthesis to provide protection against low-dose ferroptosis inducer erastin. While, TNF-α/TNFR1 facilitated ferroptosis in the presence of high-dose erastin through ROS accumulation.

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Inhibition of the NADPH Oxidase Pathway Reduces Ferroptosis during Septic Renal Injury in Diabetic Mice

Cited by 32 publications

References 33 publications

Ferroptosis in Macrophage Impairment in Sepsis

Ferroptosis in Macrophage Impairment in Sepsis

Ferroptosis inhibition attenuates inflammatory response in mice with acute hypertriglyceridemic pancreatitis

Interaction between ferroptosis and TNF‐α: Impact in obesity‐related osteoporosis

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