Vascular and valvular calcification biomarkers

Clemente, Alberto; Traghella, Irene; Mazzone, Annamaria; Sbrana, S.; Vassalle, Cristina

doi:10.1016/bs.acc.2019.08.002

Cited by 32 publications

(25 citation statements)

References 119 publications

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“…The concept that the development of atherosclerosis and heart valve disease is interrelated was a matter of debate during the last decade [ 24 , 25 , 26 , 27 ]. The arguments include common genetic susceptibility loci [ 28 , 29 , 30 ] and a number of identical circulating biomarkers [ 31 , 32 , 33 ]; yet, the similarities and differences in the pathophysiology of atherosclerosis, CAVD, and structural degeneration of BHVs have not been systematically compared. In particular, there are a lack of ultrastructural data connecting the pathophysiology of these disorders with their clinical manifestations.…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural Pathology of Atherosclerosis, Calcific Aortic Valve Disease, and Bioprosthetic Heart Valve Degeneration: Commonalities and Differences

Kostyunin

Mukhamadiyarov

Глушкова

et al. 2020

IJMS

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Atherosclerosis, calcific aortic valve disease (CAVD), and bioprosthetic heart valve degeneration (alternatively termed structural valve deterioration, SVD) represent three diseases affecting distinct components of the circulatory system and their substitutes, yet sharing multiple risk factors and commonly leading to the extraskeletal calcification. Whereas the histopathology of the mentioned disorders is well-described, their ultrastructural pathology is largely obscure due to the lack of appropriate investigation techniques. Employing an original method for sample preparation and the electron microscopy visualisation of calcified cardiovascular tissues, here we revisited the ultrastructural features of lipid retention, macrophage infiltration, intraplaque/intraleaflet haemorrhage, and calcification which are common or unique for the indicated types of cardiovascular disease. Atherosclerotic plaques were notable for the massive accumulation of lipids in the extracellular matrix (ECM), abundant macrophage content, and pronounced neovascularisation associated with blood leakage and calcium deposition. In contrast, CAVD and SVD generally did not require vasculo- or angiogenesis to occur, instead relying on fatigue-induced ECM degradation and the concurrent migration of immune cells. Unlike native tissues, bioprosthetic heart valves contained numerous specialised macrophages and were not capable of the regeneration that underscores ECM integrity as a pivotal factor for SVD prevention. While atherosclerosis, CAVD, and SVD show similar pathogenesis patterns, these disorders demonstrate considerable ultrastructural differences.

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Section: Discussionmentioning

confidence: 99%

Ultrastructural Pathology of Atherosclerosis, Calcific Aortic Valve Disease, and Bioprosthetic Heart Valve Degeneration: Commonalities and Differences

Kostyunin

Mukhamadiyarov

Глушкова

et al. 2020

IJMS

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“…Several endogenous circulating calcification inhibitors help to prevent pathophysiological mineralization. In addition, promotors and inhibitors of calcification could also serve as biomarkers for onset and progression of VC [136]. Mouse models with disrupted protective mechanisms partially feature extensive ectopic calcification.…”

Section: Absence or Dysfuntion Of Calcification Inhibitor Proteinsmentioning

confidence: 99%

Research Models for Studying Vascular Calcification

Herrmann

Babic

Tölle

et al. 2020

IJMS

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Calcification of the vessel wall contributes to high cardiovascular morbidity and mortality. Vascular calcification (VC) is a systemic disease with multifaceted contributing and inhibiting factors in an actively regulated process. The exact underlying mechanisms are not fully elucidated and reliable treatment options are lacking. Due to the complex pathophysiology, various research models exist evaluating different aspects of VC. This review aims to give an overview of the cell and animal models used so far to study the molecular processes of VC. Here, in vitro cell culture models of different origins, ex vivo settings using aortic tissue and various in vivo disease-induced animal models are summarized. They reflect different aspects and depict the (patho)physiologic mechanisms within the VC process.

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“…An osteoblast-like phenotypic transition of VSMCs and valvular interstitial cells (VICs) contributes directly to ectopic calcium deposition, respectively (83,84). Both the vascular and valvular calcifications are clinically associated with the presence of diabetes, smoking, hypertension, and dyslipidemia (84). Experimental evidence demonstrates that oxidative stress has been verified to participate in pathological vascular and valvular calcification for a long time (85)(86)(87).…”

Section: Role Of Iron In Calcific Vascular and Valvular Diseasementioning

confidence: 99%

Iron in Cardiovascular Disease: Challenges and Potentials

Zhang

2021

Front. Cardiovasc. Med.

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Iron is essential for many biological processes. Inadequate or excess amount of body iron can result in various pathological consequences. The pathological roles of iron in cardiovascular disease (CVD) have been intensively studied for decades. Convincing data demonstrated a detrimental effect of iron deficiency in patients with heart failure and pulmonary arterial hypertension, but it remains unclear for the pathological roles of iron in other cardiovascular diseases. Meanwhile, ferroptosis is an iron-dependent cell death that is distinct from apoptosis, necroptosis, and other types of cell death. Ferroptosis has been reported in several CVDs, namely, cardiomyopathy, atherosclerotic cardiovascular disease, and myocardial ischemia/reperfusion injury. Iron chelation therapy seems to be an available strategy to ameliorate iron overload-related disorders. It is still a challenge to accurately clarify the pathological roles of iron in CVD and search for effective medical intervention. In this review, we aim to summarize the pathological roles of iron in CVD, and especially highlight the potential mechanism of ferroptosis in these diseases.

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Vascular and valvular calcification biomarkers

Cited by 32 publications

References 119 publications

Ultrastructural Pathology of Atherosclerosis, Calcific Aortic Valve Disease, and Bioprosthetic Heart Valve Degeneration: Commonalities and Differences

Ultrastructural Pathology of Atherosclerosis, Calcific Aortic Valve Disease, and Bioprosthetic Heart Valve Degeneration: Commonalities and Differences

Research Models for Studying Vascular Calcification

Iron in Cardiovascular Disease: Challenges and Potentials

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