Innate and adaptive immunity in cardiovascular calcification

Passos, Lívia Silva Araújo; Lupieri, Adrien; Becker-Greene, Dakota; Aikawa, Elena

doi:10.1016/j.atherosclerosis.2020.02.016

Cited by 53 publications

(55 citation statements)

References 133 publications

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“…Autoimmune valvular carditis are mainly described in literature as associated with human rheumatic conditions, however, it is possible that autoreactive antibodies can be associated with pathology of other HVD, including CAVD. Ectopic calcification and autoimmunity has been also explored in atherosclerosis ( 21 , 22 ).…”

Section: Mechanisms Of Mitral Valve Diseasementioning

confidence: 99%

“…In addition, unlike to some of the cross-reactive intracellular proteins, GlcNac are cell-surface antigens that are more exposed/accessible to antibody recognition ( 27 ). In non-rheumatic valve disease, the triggering factors leading to cardiovascular calcification, as in CAVD are still under investigation ( 22 ).…”

Section: Mechanisms Of Mitral Valve Diseasementioning

confidence: 99%

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Rheumatic Heart Valve Disease Pathophysiology and Underlying Mechanisms

Passos

Nunes

Aïkawa

2021

Front. Cardiovasc. Med.

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Rheumatic heart valve disease (RHVD) is a post-infectious sequel of acute rheumatic fever resulting from an abnormal immune response to a streptococcal pharyngitis that triggers valvular damage. RHVD is the leading cause of cardiovascular death in children and young adults, mainly in women from low and middle-income countries. It is known that long-term inflammation and high degree of fibrosis leads to valve dysfunction due to anatomic disruption of the valve apparatus. However, since public and private investments in RHVD studies are practically inexistent the number of publications is scarce. This disease shows different natural history and clinical presentations as compared to other degenerative heart valve diseases. Although more than five decades passed after the pioneering studies on the pathogenesis of RHVD, it is still unclear how self-tolerance mechanisms fail in this disease, and how humoral and cellular inflammatory responses are interconnected. Despite that pathological mechanisms have been already proposed for RHVD, none of them are able to explain the preferential involvement of the mitral valve. This review focuses on pathophysiology and underlying mechanisms of RHVD.

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Section: Mechanisms Of Mitral Valve Diseasementioning

confidence: 99%

Section: Mechanisms Of Mitral Valve Diseasementioning

confidence: 99%

Rheumatic Heart Valve Disease Pathophysiology and Underlying Mechanisms

Passos

Nunes

Aïkawa

2021

Front. Cardiovasc. Med.

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“…Most immunity components (macrophages, dendritic cells, mast cells, neutrophils, NK cells, B cells and T cells) seem to play a role especially during preclinical microcalcifications, during which they display pro-angiogenic and pro-osteogenic activity ([ 33 ]; for extensive review see Ref. [ 34 ]). In particular, histological studies showed that oxidized lipid species activate innate immune response through toll-like receptors (TLRs) and the NF-κB pathway [ 35 ].…”

Section: The Role Of Inflammation and Oxidative Stress In The Onsementioning

confidence: 99%

Extracellular Matrix in Calcific Aortic Valve Disease: Architecture, Dynamic and Perspectives

Vito

Donato

Presta

et al. 2021

IJMS

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Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in developed countries and in the ageing population. It is strongly correlated to median age, affecting up to 13% of the population over the age of 65. Pathophysiological analysis indicates CAVD as a result of an active and degenerative disease, starting with sclerosis and chronic inflammation and then leaflet calcification, which ultimately can account for aortic stenosis. Although CAVD has been firstly recognized as a passive event mostly resulting from a degenerative aging process, much evidences suggests that calcification arises from different active processes, involving both aortic valve-resident cells (valve endothelial cells, valve interstitial cells, mesenchymal stem cells, innate immunity cells) and circulating cells (circulating mesenchymal cells, immunity cells). Moreover, a role for the cell-derived “matrix vesicles” and extracellular matrix (ECM) components has also been recognized. The aim of this work is to review the cellular and molecular alterations occurring in aortic valve during CAVD pathogenesis, focusing on the role of ECM in the natural course of the disease.

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“…Bars marked with different letters (a-e) indicate statistically significant differences (p < .05) (n ¼ 10). (Chilakapati et al, 2020;Passos et al, 2020). The findings of the current study revealed that the IL-4 and IFN-c concentrations in the anti-DEC-205-EUPS-OVA-LPSM group were notably greater than the other groups.…”

Section: Effects Of the Anti-dec-205-eups-ova-lpsm On Serum Cytokine mentioning

confidence: 42%

“…Typically, Th1-cytokines such as IFN-γ, IL-2 can promote lymphocytes division and proliferation, DC maturation, and activate Th1-based immune responses (Zivcec et al., 2020 ). Th2 cytokines, such as IL-4, −6, and −10, promote Th2-type immune responses and enhance antibody production (Chilakapati et al., 2020 ; Passos et al., 2020 ). The findings of the current study revealed that the IL-4 and IFN-γ concentrations in the anti-DEC-205-EUPS-OVA-LPSM group were notably greater than the other groups.…”

Section: Resultsmentioning

confidence: 99%