IL-18 Promotes Erythrophagocytosis and Erythrocyte Degradation by M1 Macrophages in a Calcific Microenvironment

Xu, Ran; Zhu, Dan; Guo, Jianghong; Wang, Chong

doi:10.1016/j.cjca.2021.04.007

Cited by 13 publications

(10 citation statements)

References 24 publications

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“…Many studies showed iron accumulation in IH areas. Our previous research also reported that IL-18 promotes erythrophagocytosis and erythrocyte degradation to aggravate iron overload [8]. Moreover, oxidative stress induces ferroptosis [9], which also participates in the progression of CAVD [1].…”

Section: Manuscript Text Introductionmentioning

confidence: 82%

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Iron promotes Slc7a11-deficient valvular interstitial cell osteogenic differentiation: A possible mechanism by which ferroptosis participates in intraleaflet hemorrhage-induced calcification

Huang

Zhu

et al. 2022

Free Radical Biology and Medicine

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Section: Manuscript Text Introductionmentioning

confidence: 82%

“…The extended methods of tissue delivery and storage were performed according to a previous study [8].…”

Section: Aortic Valve Collectionmentioning

confidence: 99%

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Iron promotes Slc7a11-deficient valvular interstitial cell osteogenic differentiation: A possible mechanism by which ferroptosis participates in intraleaflet hemorrhage-induced calcification

Huang

Zhu

et al. 2022

Free Radical Biology and Medicine

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“…As most studies on disease-related m6A modification have focused on many tumors, the impact of m6A regulators on the IME in AVC tissue may help us to understand disease development and disease-related immune infiltration and to establish more effective therapeutic regimens. Xu et al ( 46 ) found that IL-18 stimulates M1 macrophage-mediated erythrophagocytosis and erythrocyte breakdown by activating HO-1 and FPN through p38 and Erk1/2 in a calcific microenvironment. Additional, recent findings demonstrate an adaptive immune response functions in AVC by activating circulating CD8 + cells, their clonal proliferation and differentiation to the memory-effector subtype, and exchanges of these T-cell clones between the peripheral blood and valve ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Modification of m6A mediates tissue immune microenvironment in calcific aortic valve disease

Chen¹,

Xiong²,

Sun³

et al. 2022

Ann Transl Med

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Background: Several human diseases are associated with aberrant expression of regulators involved in N6methyladenosine (m6A) RNA modification. However, their role in aortic valve calcification (AVC) is largely unknown. The aim of this study was to determine the general expression pattern and potential function of m6A regulators in AVC by bioinformatics methods. Methods:We obtained AVC datasets from the Gene Expression Omnibus (GEO). The identification of m6Arelated differentially expressed genes (DEGs) and the Consensus Clustering method was performed to type AVC individuals based DEGs. Then, we quantified the effect of typing by principal component analysis (PCA). Next, we performed the weighted gene co-expression network analysis (WGCNA) and identified the main modules as well as functional analysis. Additionally, the key genes were screened by protein-protein interaction network (PPIN) analysis and identifying important genes of important modules. We again typed AVC individuals by the same method using key genes. Finally, we evaluated the link between key genes and immune infiltration.Results: We discovered that METTL14, ZC3H13, FTO, FMR1, HNRNPA2B1, HNRNPC, LRPPRC, YTHDC1, YTHDC2, and YTHDF1 expression levels decreased considerably in AVC tissues. Based on 10 genes, we typed 240 AVC samples as clusters A and B. We assessed the immune cell content in 240 samples using Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT) and found that B cell memory, CD8 T cells, T follicular helper cells, monocytes, M0 macrophages, resting dendritic cells (DCs), and interleukin-10 (IL-10) were concentrated in the cluster A group. Additionally, based on the important WGCNA modules, we identified 7 key genes. Next, 240 samples were retyped based on 7 key genes; we found that T cells CD8, T cells CD4 memory activated, T cells follicular helper, and macrophages M1 were significantly increased in gene cluster-1. Finally, we performed functional enrichment of gene cluster-typed samples, showing potential functional differences between different types. Conclusions:Our study provides a review of the m6A regulators' expression pattern and functional importance in human AVC. The data from this study might serve as a significant resource for future mechanistic and therapeutic investigations into the role of critical m6A regulators in AVC.

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“…Pathological hemophagocytosis was also proposed in the etiology of Leishmania-triggered anemia and was linked to SIRPα downregulation [147]. Another report described hemophagocytosis in calcified vascular walls and implicated IL-18 as a signal that promoted this phenomenon [148].…”

Section: Development and Plasticity Of Iron-recycling Macrophagesmentioning

confidence: 99%

The Multiple Facets of Iron Recycling

Slusarczyk

Mleczko-Sanecka

2021

Genes

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The production of around 2.5 million red blood cells (RBCs) per second in erythropoiesis is one of the most intense activities in the body. It continuously consumes large amounts of iron, approximately 80% of which is recycled from aged erythrocytes. Therefore, similar to the “making”, the “breaking” of red blood cells is also very rapid and represents one of the key processes in mammalian physiology. Under steady-state conditions, this important task is accomplished by specialized macrophages, mostly liver Kupffer cells (KCs) and splenic red pulp macrophages (RPMs). It relies to a large extent on the engulfment of red blood cells via so-called erythrophagocytosis. Surprisingly, we still understand little about the mechanistic details of the removal and processing of red blood cells by these specialized macrophages. We have only started to uncover the signaling pathways that imprint their identity, control their functions and enable their plasticity. Recent findings also identify other myeloid cell types capable of red blood cell removal and establish reciprocal cross-talk between the intensity of erythrophagocytosis and other cellular activities. Here, we aimed to review the multiple and emerging facets of iron recycling to illustrate how this exciting field of study is currently expanding.

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IL-18 Promotes Erythrophagocytosis and Erythrocyte Degradation by M1 Macrophages in a Calcific Microenvironment

Cited by 13 publications

References 24 publications

Iron promotes Slc7a11-deficient valvular interstitial cell osteogenic differentiation: A possible mechanism by which ferroptosis participates in intraleaflet hemorrhage-induced calcification

Iron promotes Slc7a11-deficient valvular interstitial cell osteogenic differentiation: A possible mechanism by which ferroptosis participates in intraleaflet hemorrhage-induced calcification

Modification of m6A mediates tissue immune microenvironment in calcific aortic valve disease

The Multiple Facets of Iron Recycling

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