Endothelial transferrin receptor 1 contributes to thrombogenesis through cascade ferroptosis

Ma, Haotian; Huang, Yongtao; Tian, Wenrong; Liu, Jincen; Yan, Xinyue; Ma, Lei; Lai, Jianghua

doi:10.1016/j.redox.2024.103041

Cited by 3 publications

(1 citation statement)

References 59 publications

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“…VT results from the interaction of various factors, such as vascular endothelial cells [ 11 ], platelets [ 12 ], coagulation function [ 13 ], and the fibrinolytic system [ 14 ], all of which undergo varying degrees of change before thrombosis [ 15 ]. Therefore, it is crucial to implement appropriate interventions to hinder VT development and to identify early screening and diagnostic methods.…”

Section: Discussionmentioning

confidence: 99%

Discovery of crucial cytokines associated with deep vein thrombus formation by protein array analysis

Wang,

Chi,

Zeng

et al. 2024

BMC Cardiovasc Disord

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Background Expanding the number of biomarkers is imperative for studying the etiology and improving venous thromboembolism prediction. In this study, we aimed to identify promising biomarkers or targeted therapies to improve the detection accuracy of early-stage deep vein thrombosis (DVT) or reduce complications. Methods Quantibody Human Cytokine Antibody Array 440 (QAH-CAA-440) was used to screen novel serum-based biomarkers for DVT/non-lower extremity DVT (NDVT). Differentially expressed proteins in DVT were analyzed using bioinformatics methods and validated using a customized array. Diagnostic accuracy was calculated using receiver operating characteristics, and machine learning was applied to establish a biomarker model for evaluating the identified targets. Twelve targets were selected for validation. Results Cytokine profiling was conducted using a QAH-CAA-440 (RayBiotech, USA) quantimeter array. Cross-tabulation analysis with Venn diagrams identified common differential factors, leading to the selection of 12 cytokines for validation based on their clinical significance. These 12 biomarkers were consistent with the results of previous array analysis: FGF-6 (AUC = 0.956), Galectin-3 (AUC = 0.942), EDA-A2 (AUC = 0.933), CHI3L1 (AUC = 0.911), IL-1 F9 (AUC = 0.898), Dkk-4 (AUC = 0.88), IG-H3 (AUC = 0.876), IGFBP (AUC = 0.858), Gas-1 (AUC = 0.858), Layilin (AUC = 0.849), ULBP-2 (AUC = 0.813)and FGF-9 (AUC = 0.773). These cytokines are expected to serve as biomarkers, targets, or therapeutic targets to differentiate DVT from NDVT. Conclusions EDA-A2, FGF-6, Dkk-4, IL-1 F9, Galentin-3, Layilin, Big-h3, CHI3L1, ULBP-2, Gas-1, IGFBP-5, and FGF-9 are promising targets for DVT diagnosis and treatment.

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Section: Discussionmentioning

confidence: 99%

Discovery of crucial cytokines associated with deep vein thrombus formation by protein array analysis

Wang,

Chi,

Zeng

et al. 2024

BMC Cardiovasc Disord

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Rosmarinic acid liposomes suppress ferroptosis in ischemic brain via inhibition of TfR1 in BMECs

Jia,

Gou,

Gao

et al. 2024

Phytomedicine

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Ferroptosis and Its Potential Role in the Physiopathology of Skeletal Muscle Atrophy

Sun,

Xiao,

Sun

et al. 2024

IJMS

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Skeletal muscle atrophy is a major health concern, severely affecting the patient’s mobility and life quality. In the pathological process of skeletal muscle atrophy, with the progressive decline in muscle quality, strength, and function, the incidence of falling, fracture, and death is greatly increased. Unfortunately, there are no effective treatments for this devastating disease. Thus, it is imperative to investigate the exact pathological molecular mechanisms underlying the development of skeletal muscle atrophy and to identify new therapeutic targets. Decreased muscle mass, strength, and muscle fiber cross-sectional area are typical pathological features and manifestations of skeletal muscle atrophy. Ferroptosis, an emerging type of programmed cell death, is characterized by iron-dependent oxidative damage, lipid peroxidation, and reactive oxygen species accumulation. Notably, the understanding of its role in skeletal muscle atrophy is emerging. Ferroptosis has been found to play an important role in the intricate interplay between the pathological mechanisms of skeletal muscle atrophy and its progression caused by multiple factors. This provides new opportunities and challenges in the treatment of skeletal muscle atrophy. Therefore, we systematically elucidated the ferroptosis mechanism and its progress in skeletal muscle atrophy, aiming to provide a comprehensive insight into the intricate relationship between ferroptosis and skeletal muscle atrophy from the perspectives of iron metabolism and lipid peroxidation and to provide new insights for targeting the pathways related to ferroptosis and the treatment of skeletal muscle atrophy.

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Endothelial transferrin receptor 1 contributes to thrombogenesis through cascade ferroptosis

Cited by 3 publications

References 59 publications

Discovery of crucial cytokines associated with deep vein thrombus formation by protein array analysis

Discovery of crucial cytokines associated with deep vein thrombus formation by protein array analysis

Rosmarinic acid liposomes suppress ferroptosis in ischemic brain via inhibition of TfR1 in BMECs

Ferroptosis and Its Potential Role in the Physiopathology of Skeletal Muscle Atrophy

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