Inhibition of Ca<sup>2+</sup>-calpain signaling is a new mechanism using <i>Laminaria japonica</i> polysaccharide to prevent macrophage foam cell formation and atherosclerosis

Li, Xueying; Kuang, Dan-Dan; Guo, An-Jun; Deng, Yuanyuan; Pan, Li‐Hua; Li, Qiang-Ming; Luo, Jian‐Ping; Zha, Xue‐Qiang

doi:10.1039/d2fo04099a

Cited by 6 publications

(3 citation statements)

References 52 publications

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“…Hoving et al found that mannose oligosaccharides could prevent worsening of atherosclerosis by reducing serum cholesterol levels and that these oligosaccharides may increase the butyric acid level in the cecum and promote excretion of bile acids by influencing the gut microbiome 78 . Li et al demonstrated that polysaccharides from Laminaria japonica suppressed atherosclerosis by increasing activity in the autophagy pathway 79 . Red algal polysaccharide has been investigated and may be a potential treatment for atherosclerosis 80 .…”

Section: Treatment Of Atherosclerosismentioning

confidence: 99%

Impact of the gut microbiome on atherosclerosis

Mao,

Kong,

Zang

et al. 2024

mLife

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Atherosclerosis is a chronic inflammatory metabolic disease with a complex pathogenesis. However, the exact details of its pathogenesis are still unclear, which limits effective clinical treatment of atherosclerosis. Recently, multiple studies have demonstrated that the gut microbiota plays a pivotal role in the onset and progression of atherosclerosis. This review discusses possible treatments for atherosclerosis using the gut microbiome as an intervention target and summarizes the role of the gut microbiome and its metabolites in the development of atherosclerosis. New strategies for the treatment of atherosclerosis are needed. This review provides clues for further research on the mechanisms of the relationship between the gut microbiota and atherosclerosis.

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Section: Treatment Of Atherosclerosismentioning

confidence: 99%

Impact of the gut microbiome on atherosclerosis

Mao,

Kong,

Zang

et al. 2024

mLife

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“…LJP61A markedly reduces intracellular Ca 2+ to provoke macrophage autophagy, resulting in the suppression of lipid accumulation and AS. 135 …”

Section: Autophagy‐mediated Regulation In Macrophage Functionsmentioning

confidence: 99%

Comprehensive view of macrophage autophagy and its application in cardiovascular diseases

Pan,

Zhang,

Zhang

et al. 2023

Cell Proliferation

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Cardiovascular diseases (CVDs) are the primary drivers of the growing public health epidemic and the leading cause of premature mortality and economic burden worldwide. With decades of research, CVDs have been proven to be associated with the dysregulation of the inflammatory response, with macrophages playing imperative roles in influencing the prognosis of CVDs. Autophagy is a conserved pathway that maintains cellular functions. Emerging evidence has revealed an intrinsic connection between autophagy and macrophage functions. This review focuses on the role and underlying mechanisms of autophagy‐mediated regulation of macrophage plasticity in polarization, inflammasome activation, cytokine secretion, metabolism, phagocytosis, and the number of macrophages. In addition, autophagy has been shown to connect macrophages and heart cells. It is attributed to specific substrate degradation or signalling pathway activation by autophagy‐related proteins. Referring to the latest reports, applications targeting macrophage autophagy have been discussed in CVDs, such as atherosclerosis, myocardial infarction, heart failure, and myocarditis. This review describes a novel approach for future CVD therapies.

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“…Frequently classified as a macrophage subtype, foam cells exhibit persistent residence within plaques, thereby contributing to the disease's progression 5 . Intracellular Ca 2+ overload in macrophages is identified as a powerful stimulant for oxidative stress and inflammatory responses, which in turn, aggravate atherosclerotic plaque formation and advancement 6 . Consequently, the assessment of intracellular Ca 2+ concentrations is fundamentally crucial to comprehend the pathophysiological mechanisms underpinning atherosclerosis development 7 …”

Section: Introductionmentioning

confidence: 99%

Moxibustion's protective role against atherosclerosis: Inhibition of Ca²⁺ overload‐triggered oxidative stress and inflammatory response via P2Y12/PI3K/AKT pathway

Yang,

Liu,

et al. 2023

Environmental Toxicology

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ObjectiveThis study aims to investigate the protective mechanism of moxibustion in combating atherosclerosis (AS).MethodsApolipoprotein E (ApoE)‐deficient mice, aged 8 weeks, were randomly assigned into four groups: the model group (n = 6), SC79 group (n = 6), moxibustion group (n = 6), and moxibustion+SC79 group (n = 6). All mice were fed with a high‐fat diet (HFD). Concurrently, 8‐week‐old C57BL/6 mice of the same genetic background were utilized as the control group (n = 6) and were given a regular diet. Macrophages were isolated via flow cytometry. The intracellular Ca2+ expression in macrophages was evaluated, and aortic plaques were quantitatively assessed through en face oil red O and Masson staining. The presence of macrophages and smooth muscle cells in AS plaques was determined by MAC‐3 and α‐smooth muscle actin (α‐SMA) immunohistochemistry. The relative fluorescence intensity of nuclear factor‐κB (NF‐κB) in macrophages was identified by immunofluorescence staining. The expressions of proteins related to the P2Y12/phosphatidylinositol 3‐hydroxy kinase (PI3K)/protein kinase B (AKT) signaling pathway were examined by Western blotting.ResultsMoxibustion reduced free Ca2+ expression in macrophage cytoplasm, inhibiting Ca2+ influx and oxidative stress. Significant reductions in atherosclerotic plaque formation and inflammation markers, including TNF‐α and IL‐1β, were noted in the moxibustion group. Moxibustion modulated the P2Y12/PI3K/AKT pathway, impacting various inflammatory and oxidative stress‐related proteins. Introduction of the AKT activator SC79 counteracted moxibustion's benefits, highlighting the P2Y12/PI3K/AKT pathway's central role.ConclusionMoxibustion, through the P2Y12/PI3K/AKT signaling pathway, can inhibit Ca2+ overload‐induced oxidative stress and inflammatory response, decrease macrophage infiltration, and increase the content of smooth muscle cells and collagen, thereby exerting a protective effect against AS.

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Inhibition of Ca²⁺-calpain signaling is a new mechanism using Laminaria japonica polysaccharide to prevent macrophage foam cell formation and atherosclerosis

Abstract: The LJP61A suppressed macrophage foam cell formation and atherosclerotic progression by modulating Ca2+-calpain mediated autophagy inhibition.

Cited by 6 publications

References 52 publications

Impact of the gut microbiome on atherosclerosis

Impact of the gut microbiome on atherosclerosis

Comprehensive view of macrophage autophagy and its application in cardiovascular diseases

Moxibustion's protective role against atherosclerosis: Inhibition of Ca²⁺ overload‐triggered oxidative stress and inflammatory response via P2Y12/PI3K/AKT pathway

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Inhibition of Ca2+-calpain signaling is a new mechanism using Laminaria japonica polysaccharide to prevent macrophage foam cell formation and atherosclerosis

Abstract: The LJP61A suppressed macrophage foam cell formation and atherosclerotic progression by modulating Ca2+-calpain mediated autophagy inhibition.

Cited by 6 publications

References 52 publications

Impact of the gut microbiome on atherosclerosis

Impact of the gut microbiome on atherosclerosis

Comprehensive view of macrophage autophagy and its application in cardiovascular diseases

Moxibustion's protective role against atherosclerosis: Inhibition of Ca2+ overload‐triggered oxidative stress and inflammatory response via P2Y12/PI3K/AKT pathway

Contact Info

Product

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Inhibition of Ca²⁺-calpain signaling is a new mechanism using Laminaria japonica polysaccharide to prevent macrophage foam cell formation and atherosclerosis

Moxibustion's protective role against atherosclerosis: Inhibition of Ca²⁺ overload‐triggered oxidative stress and inflammatory response via P2Y12/PI3K/AKT pathway