Research Progress of Ferroptosis in Adiposity-Based Chronic Disease (ABCD)

Du, Huijun; Ren, Xiaoying; Bai, Juncai; Yang, Wei; Gao, Yunan; Yan, Shuang

doi:10.1155/2022/1052699

Cited by 13 publications

(12 citation statements)

References 65 publications

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“…This review summarizes the characteristics of iron metabolism in humans, the association between obesity and ferroptosis, and the neuroimmune regulation associated with obesity and ferroptosis. While many of these mechanisms are still unknown, there is growing evidence that ferroptosis plays a key role in obesity and its complications, including type II diabetes, hypertension, nonalcoholic steatohepatitis, atherosclerosis, and obese cardiomyopathy ( 171 ). Moreover, ferroptosis may not only play a direct role in AT, but also indirectly promote the development of obesity through the inflammatory response and insulin resistance caused by liver autonomic and immunomodulatory disorders( Figure 4 ).…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

et al. 2022

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Ferroptosis requires not only the accumulation of iron ions, but also changes in many ferroptosis-related regulators, including a decrease in GPX4 and inhibition of SLC7A11 for classical ferroptosis, a deletion of FSP1 or GCH1. Surprisingly, adipose tissue (AT) in the obesity conditions is also accompanied by iron buildup, decreased GSH, and increased ROS. On the neurological side, the pro-inflammatory factor released by AT may have first caused ferroptosis in the vagus nerve by inhibiting of the NRF2-GPX4 pathway, resulting in disorders of the autonomic nervous system. On the immune side, obesity may cause M2 macrophages ferroptosis due to damage to iron-rich ATMs (MFehi) and antioxidant ATMs (Mox), and lead to Treg cells ferroptosis through reductions in NRF2, GPX4, and GCH1 levels. At the same time, the reduction in GPX4 may also trigger the ferroptosis of B1 cells. In addition, some studies have also found the role of GPX4 in neutrophil autophagy, which is also worth pondering whether there is a connection with ferroptosis. In conclusion, this review summarizes the associations between neuroimmune regulation associated with obesity and ferroptosis, and on the basis of this, highlights their potential molecular mechanisms, proposing that ferroptosis in one or more cells in a multicellular tissue changes the fate of that tissue.

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Section: Discussionmentioning

confidence: 99%

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

et al. 2022

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“…Since ferroptosis was associated with lipid peroxidation, the dynamic change of lipid peroxidation is also involved in the development of obesity-related cardiomyopathy. Palmitic acid was found to inhibit the protein expression levels of GPX4 in a dose-and time-dependent manner and was restored by different ferroptosis inhibitors in vitro study (57). A recent study revealed that obese adipose tissue macrophages (ATMs) derived exosomes resulted in ferroptosis via glutathione synthesis disorder by targeting SLC7A11 in obesity-induced cardiac injury (58).…”

Section: Heart Failurementioning

confidence: 99%

Mapping current research and identifying hotspots of ferroptosis in cardiovascular diseases

Teng

Kong

Huang

et al. 2022

Front. Cardiovasc. Med.

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ObjectiveFerroptosis is a unique cell death depended on iron metabolism disorder which is different from previous apoptosis-regulated cell death. Early studies have proposed that ferroptosis is closely associated with multiple cardiovascular diseases (CVDs). However, the relationship of ferroptosis and CVDs has not been summarized by using bibliometric analysis. We intended to illustrate the development of ferroptosis in CVDs over the past years and provide relevant valuable information.Materials and methodsThe authoritative database of Web of Science Core Collection was collected for retrieving ferroptosis studies in CVDs. In this work, statistical and visualization analysis were conducted using VOSviewer and Citespace.ResultsA total of 263 studies were included in the final study. From the perspective of the overall literature, the study maintains an increased trend year by year and most manuscripts belonged to original article. China was the most productive country with the utmost scientific research output, as well as the institutions and authors, followed by Germany and the United States of America (USA). Jun Peng from China contributes to the most publications. Collaborative efforts between institutes and authors were limited and there was little widespread cooperation. In addition, burst keywords analysis discovered that ischemia-reperfusion (I/R) injury, heart failure (HF), and atherosclerosis were the top three research directions of ferroptosis in CVDs. The burst investigation and timeline views also indicated that endothelial injury and gut microbiota may also serve as new research topics in the future.ConclusionThis study provided comprehensive and specific information about the most influential articles on ferroptosis in CVDs. The relationship between ferroptosis and CVDs had attracted the scholar’s concerns especially in China. Cooperations and communications between countries and institutions should be emphasized and future directions can be concentrated on endothelial disorder and gut microbiota.

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“…In recent years, the relationship between iron and PNI has attracted increasing attention. In normal conditions, the system xc --GSH-GPX4 axis is responsible for the extracellular transport of cystine and the intracellular transport of glutamat [103]. A microenvironment is established upon nerve injury, which consists of axons, SCs, blood vessels, inflammatory factors and cells, extracellular matrix, and connective tissue [104].…”

Section: Ferroptosis and Peripheral Nerve Injurymentioning

confidence: 99%

Iron Metabolism and Ferroptosis in Peripheral Nerve Injury

Huang

Bian

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Peripheral nerve injury (PNI) is a major clinical problem that may lead to different levels of sensory and motor dysfunction including paralysis. Due to the high disability rate and unsatisfactory prognosis, the exploration and revealment of the mechanisms involved in the PNI are urgently required. Ferroptosis, a recently identified novel form of cell death, is an iron-dependent process. It is a unique modality of cell death, closely associated with iron concentrations, generation of reactive oxygen species, and accumulation of the lipid reactive oxygen species. These processes are regulated by multiple cellular metabolic pathways, including iron overloading, lipid peroxidation, and the glutathione/glutathione peroxidase 4 pathway. Furthermore, ferroptosis is accompanied by morphological changes in the mitochondria, such as increased membrane density and shrunken mitochondria; this association between ferroptosis and mitochondrial damage has been detected in various diseases, including spinal cord injury and PNI. The inhibition of ferroptosis can promote the repair of damaged peripheral nerves, reduce mitochondrial damage, and promote the recovery of neurological function. In this review, we intend to discuss the detailed mechanisms of ferroptosis and summarize the current researches on ferroptosis with respect to nerve injury. This review also aims at providing new insights on targeting ferroptosis for PNI treatment.

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Research Progress of Ferroptosis in Adiposity-Based Chronic Disease (ABCD)

Cited by 13 publications

References 65 publications

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system

Mapping current research and identifying hotspots of ferroptosis in cardiovascular diseases

Iron Metabolism and Ferroptosis in Peripheral Nerve Injury

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