Arterial calcification: A new perspective?

Nicoll, Rachel; Henein, Michael Y.

doi:10.1016/j.ijcard.2016.11.099

Cited by 44 publications

(29 citation statements)

References 199 publications

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“…Vascular calcification is a complex pathological process. Its development is often involved in diseases with chronic inflammatory disorders [20][21][22], such as type 2 diabetes mellitus and brain arterial stiffness [2,23]. In the central nervous system, microglia, which are the largest population of mononuclear phagocytes [24], play important roles in perivascular and pericalcification areas [25].…”

Section: Discussionmentioning

confidence: 99%

miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment

et al. 2020

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Background: Vascular calcification is often associated with chronic inflammation and is a risk factor for brain arterial stiffness. Our previous results showed that miR32-5p was positively correlated with vascular smooth muscle cells (VSMC) calcification, but it is unclear whether miR32-5p promoted VSMC calcification by regulating inflammatory factor production. Results: In this study, bioinformatics analysis was used to select tumour necrosis factor α (TNFα) as a candidate inflammatory factor associated with calcification. Moreover, alizarin red staining and qRT-PCR analysis revealed that TNFα produced by BV2 cells was the key promoting factor of VSMC calcification. Interestingly, the expression of TNFα was significantly increased at the mRNA and protein levels after miR32-5p mimic treatment but significantly decreased after miR32-5p antagomir treatment. To explore the mechanism of the regulation of TNFα expression by miR32-5p, bioinformatics analysis indicated that PIKfyve was a candidate target gene of miR32-5p, and luciferase assays verified that the expression of PIKfyve was significantly repressed by miR32-5p mimics. Importantly, rescue experiments showed that the expression of TNFα in BV2 cells treated with miR32-5p antagomir and the PIKfyve inhibitor YM201636 was significantly increased. Conclusions: The production of TNFα in microglia could be affected by miR32-5p targeting PIKfyve, and these results will be beneficial to reveal the mechanism of brain arterial calcification.

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Section: Discussionmentioning

confidence: 99%

miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment

et al. 2020

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“…This is confirmed by the observation that the use of statins, which are known to reduce vascular inflammation [57,58], is associated with increased plaque calcification and fibrous cap thickness, resulting in stabilization of the atherosclerotic lesions [59][60][61][62][63][64][65]. Moreover, recent data have shown that the degree of coronary artery calcification is significantly higher in symptomatic patients who had chronic coronary artery disease compared to patients who sustained acute coronary events [43,66,67]. In asymptomatic patients with type 2 diabetes, the plaques more likely to become culprit plaques for acute coronary events over a 8-year follow-up were characterized by larger volume, greater lipid content, and only mild calcification [68].…”

Section: Pathologymentioning

confidence: 81%

“…Calcifications in atherosclerotic plaques develop as a healing response to intense local macrophage inflammatory and immune activity, leading also to the osteogenic transformation of vascular smooth muscle cells [42][43][44][45][46]. In lesions with extensive inflammation, macrophage-derived vesicles are released within the necrotic core of the plaque and serve as nucleating sites for calcification [47][48][49].…”

Section: Pathologymentioning

confidence: 99%

Coronary Artery Microcalcification: Imaging and Clinical Implications

Vancheri¹,

Longo²,

Vancheri

et al. 2019

Diagnostics

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Strategies to prevent acute coronary and cerebrovascular events are based on accurate identification of patients at increased cardiovascular (CV) risk who may benefit from intensive preventive measures. The majority of acute CV events are precipitated by the rupture of the thin cap overlying the necrotic core of an atherosclerotic plaque. Hence, identification of vulnerable coronary lesions is essential for CV prevention. Atherosclerosis is a highly dynamic process involving cell migration, apoptosis, inflammation, osteogenesis, and intimal calcification, progressing from early lesions to advanced plaques. Coronary artery calcification (CAC) is a marker of coronary atherosclerosis, correlates with clinically significant coronary artery disease (CAD), predicts future CV events and improves the risk prediction of conventional risk factors. The relative importance of coronary calcification, whether it has a protective effect as a stabilizing force of high-risk atherosclerotic plaque has been debated until recently. The extent of calcium in coronary arteries has different clinical implications. Extensive plaque calcification is often a feature of advanced and stable atherosclerosis, which only rarely results in rupture. These macroscopic vascular calcifications can be detected by computed tomography (CT). The resulting CAC scoring, although a good marker of overall coronary plaque burden, is not useful to identify vulnerable lesions prone to rupture. Unlike macrocalcifications, spotty microcalcifications assessed by intravascular ultrasound or optical coherence tomography strongly correlate with plaque instability. However, they are below the resolution of CT due to limited spatial resolution. Microcalcifications develop in the earliest stages of coronary intimal calcification and directly contribute to plaque rupture producing local mechanical stress on the plaque surface. They result from a healing response to intense local macrophage inflammatory activity. Most of them show a progressive calcification transforming the early stage high-risk microcalcification into the stable end-stage macroscopic calcification. In recent years, new developments in noninvasive cardiovascular imaging technology have shifted the study of vulnerable plaques from morphology to the assessment of disease activity of the atherosclerotic lesions. Increased disease activity, detected by positron emission tomography (PET) and magnetic resonance (MR), has been shown to be associated with more microcalcification, larger necrotic core and greater rates of events. In this context, the paradox of increased coronary artery calcification observed in statin trials, despite reduced CV events, can be explained by the reduction of coronary inflammation induced by statin which results in more stable macrocalcification.

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“…The aim of performing imaging diagnostic tests is the assessment of patients at risk of acute coronary events associated with plaque formation, before atherosclerotic complications occur. This objective is based on the identification of coronary Although postmortem studies suggest that TCFA are most often found in the culprit lesions in acute coronary syndrome, the majority of vulnerable plaques undergo progressive transformation from high-risk lesions to more stable plaques with extensive calcification, while others undergo subclinical rupture and healing [34][35][36]. As a consequence, since most plaque ruptures are silent, the few that are responsible for the acute events cannot be distinguished from the others.…”

Section: Introductionmentioning

confidence: 99%

Coronary Atherosclerosis Imaging

et al. 2020

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Identifying patients at increased risk of coronary artery disease, before the atherosclerotic complications become clinically evident, is the aim of cardiovascular prevention. Imaging techniques provide direct assessment of coronary atherosclerotic burden and pathological characteristics of atherosclerotic lesions which may predict the progression of disease. Atherosclerosis imaging has been traditionally based on the evaluation of coronary luminal narrowing and stenosis. However, the degree of arterial obstruction is a poor predictor of subsequent acute events. More recent techniques focus on the high-resolution visualization of the arterial wall and the coronary plaques. Most acute coronary events are triggered by plaque rupture or erosion. Hence, atherosclerotic plaque imaging has generally focused on the detection of vulnerable plaque prone to rupture. However, atherosclerosis is a dynamic process and the plaque morphology and composition may change over time. Most vulnerable plaques undergo progressive transformation from high-risk to more stable and heavily calcified lesions, while others undergo subclinical rupture and healing. Although extensive plaque calcification is often associated with stable atherosclerosis, the extent of coronary artery calcification strongly correlates with the degree of atherosclerosis and with the rate of future cardiac events. Inflammation has a central role in atherogenesis, from plaque formation to rupture, hence in the development of acute coronary events. Morphologic plaque assessment, both invasive and non-invasive, gives limited information as to the current activity of the atherosclerotic disease. The addition of nuclear imaging, based on radioactive tracers targeted to the inflammatory components of the plaques, provides a highly sensitive assessment of coronary disease activity, thus distinguishing those patients who have stable disease from those with active plaque inflammation.

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Arterial calcification: A new perspective?

Cited by 44 publications

References 199 publications

miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment

miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment

Coronary Artery Microcalcification: Imaging and Clinical Implications

Coronary Atherosclerosis Imaging

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