Ferroptosis as a therapeutic target for inflammation-related intestinal diseases

Zhang, Xiaoli; Lv, Guoqing; Wang, Hongying

doi:10.3389/fphar.2023.1095366

Cited by 25 publications

(14 citation statements)

References 81 publications

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“…To improve patient quality of life, increase life expectancy, and lessen the burden on society, it is crucial to understand the pathogenesis of NDs and identify effective therapeutic targets. At the same time, a considerable number of studies have shown an association between the onset and progression of NDs and ferroptosis (Gallucci et al 2008 ; Wu et al 2021 ; Zhang et al 2023 ) (Fig. 1 ).…”

Section: Introductionmentioning

confidence: 92%

“…Nrf2-associated markers of ferroptosis require binding to others for specific detection and detection of cellular ferroptosis. Nevertheless, according to several studies (Habas et al 2013 ), Nrf2 has become an important therapeutic target of NDs because of its important role in protecting neurons from OS and glutamate-induced excitotoxicity and ultimately maintaining the survival of injured neurons (Zhang et al 2023 ).…”

Section: Biomarkers and Therapeutics Targeting Nrf2 And Ferroptosis I...mentioning

confidence: 99%

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Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases

Xiang,

Song,

Long

2024

Arch Toxicol

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This article provides an overview of the background knowledge of ferroptosis in the nervous system, as well as the key role of nuclear factor E2-related factor 2 (Nrf2) in regulating ferroptosis. The article takes Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS) as the starting point to explore the close association between Nrf2 and ferroptosis, which is of clear and significant importance for understanding the mechanism of neurodegenerative diseases (NDs) based on oxidative stress (OS). Accumulating evidence links ferroptosis to the pathogenesis of NDs. As the disease progresses, damage to the antioxidant system, excessive OS, and altered Nrf2 expression levels, especially the inhibition of ferroptosis by lipid peroxidation inhibitors and adaptive enhancement of Nrf2 signaling, demonstrate the potential clinical significance of Nrf2 in detecting and identifying ferroptosis, as well as targeted therapy for neuronal loss and mitochondrial dysfunction. These findings provide new insights and possibilities for the treatment and prevention of NDs.

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Section: Introductionmentioning

confidence: 92%

Section: Biomarkers and Therapeutics Targeting Nrf2 And Ferroptosis I...mentioning

confidence: 99%

Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases

Xiang,

Song,

Long

2024

Arch Toxicol

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“…Iron overload has been linked to ferroptosis, an intracellular iron-dependent form of cell death [67,70,71]. This process involves the release of damage-associated molecular patterns (DAMPs) and lipid peroxidation products, which in turn activate the NF-κB pathway, leading to inflammation [72]. Furthermore, iron overload has been correlated with increased levels of vascular endothelial growth factor A (VEGFA) and IL-8, proinflammatory cytokines described above, thus triggering inflammation through an additional mechanism [70,73,74].…”

Section: Oxidative Stressmentioning

confidence: 99%

Immune Dysregulation in Endometriomas: Implications for Inflammation

Dymanowska-Dyjak,

Terpiłowska,

Morawska-Michalska

et al. 2024

IJMS

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The most common manifestation of endometriosis, a condition characterized by the presence of endometrial-like tissue outside of the uterus, is the endometrioma, a cystic ovarian lesion. It is a commonly occurring condition associated with chronic pelvic pain exacerbated prior to and during menstruation, as well as infertility. The exact pathomechanisms of the endometrioma are still not fully understood. Emerging evidence suggests a pivotal role of immune dysregulation in the pathogenesis of endometriomas, primarily influencing both local and systemic inflammatory processes. Among the factors implicated in the creation of the inflammatory milieu associated with endometriomas, alterations in both serum and local levels of several cytokines stand out, including IL-6, IL-8, and IL-1β, along with abnormalities in the innate immune system. While numerous signaling pathways have been suggested to play a role in the inflammatory process linked to endometriomas, only NF-κB has been conclusively demonstrated to be involved. Additionally, increased oxidative stress, both resulting from and contributing to endometriomas, has been identified as a primary driver of both systemic and local inflammation associated with the condition. This article reviews the current understanding of immune dysfunctions in the endometrioma and their implications for inflammation.

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“…Among the different aldehydes that can be formed as secondary products during lipid peroxidation, malondialdehyde and 4-hydroxynonenal (4-HNE) stand out, both being associated with different stages of MAFLD [208]. In turn, arachidonic acid and adrenic acid-containing phosphatidylethanolamines (PEs), vulnerable to ROS attack, are the main substrates for lipid peroxidation; such long-chain polyunsaturated fatty acids are preferentially catalyzed to their acyl-CoA esters by long-chain acyl-CoA synthetase family member 4 (ACSL4), re-acylated into lysophospholipids by lysophosphatylcholine acyltransferase 3 (LPCAT3), and subsequently oxidized by lipoxygenase, resulting in membrane rupture and ferroptotic cell death [209].…”

Section: Ferroptosismentioning

confidence: 99%

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

De Cól,

de Lima,

Pompeu

et al. 2024

IJMS

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Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain–gut–liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain–gut–liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines.

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Ferroptosis as a therapeutic target for inflammation-related intestinal diseases

Cited by 25 publications

References 81 publications

Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases

Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases

Immune Dysregulation in Endometriomas: Implications for Inflammation

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

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