Parvovirus B19-induced angiogenesis in fulminant myocarditis

Ackermann, Maximilian; Wagner, Willi L.; Rellecke, Philipp; Akhyari, Payam; Boeken, Udo; Reinecke, Petra

doi:10.1093/eurheartj/ehaa092

Cited by 23 publications

(22 citation statements)

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“…Viral-associated thrombotic microangiopathies have been described in numerous inflammatory cardiorespiratory diseases ( e.g. influenza [ 10 ] or myocarditis [ 11 ]). We compared post-mortem lung tissues from patients who died from COVID-19 with severe ARDS and diffuse alveolar damage due to influenza A (H1N1) infection.…”

Section: Editorialmentioning

confidence: 99%

Inflammation and intussusceptive angiogenesis in COVID-19: everything in and out of flow

et al. 2020

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Section: Editorialmentioning

confidence: 99%

Inflammation and intussusceptive angiogenesis in COVID-19: everything in and out of flow

et al. 2020

Self Cite

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“…43 Moreover, IHC using cell type-specific markers can make accurate classifications and help distinguish the sub-types of infiltrated cells, such as the different T lymphocyte subtypes (CD4 + , CD8 + ), macrophage (CD68 + ), and B lymphocyte (CD20 + ). Transmission electron microscope (TEM) can provide myocardium ultrastructure information and possibly identify viral particles, 44 but technical limitations slow result acquisition and is not used as a routine test.…”

Section: Etiologymentioning

confidence: 99%

Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes

Hang

Chen

Seubert

et al. 2020

Sig Transduct Target Ther

103

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Fulminant myocarditis (FM) is characterized by a rapid progressive decline in cardiac function and a high mortality rate. Since the first report of FM patients in the 1980s, several clinical trials and research studies have been published increasing our knowledge regarding FM. Currently, the diagnosis of FM depends on various techniques including electrocardiography, echocardiography, endomyocardial biopsy, and cardiac magnetic resonance. The development of mechanical circulation support (MCS) devices and progress in our understanding of the pathophysiological mechanisms underlying FM, treatment regimens have evolved from simple symptomatic treatment to a life support-based comprehensive treatment approach. The core mechanism underlying the development of FM is the occurrence of an inflammatory cytokine storm. This review provides a comprehensive account of the current understanding of FM pathophysiology and knowledge regarding its etiology, pathophysiology, treatments, and outcomes.

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“…The Orf virus, a zoonotic parapoxvirus that may be transmitted to humans, rarely provokes an extensive vasculo-endothelial proliferation through the early expression of a VEGF-like viral gene product [ 9 ]. Moreover, despite the infection of fibroblasts by parvovirus B19 has been suggested to have anti-angiogenic effects in vitro [ 10 ], it has been recently reported [ 11 ] that parvovirus B19-related induction of myocarditis caused a distinct formation of new blood vessels around inflammatory sites both by SA and IA. An anti-angiogenic effect has been instead observed in other viral models: Zika virus (ZIKV), besides neurogenesis, also seems impair angiogenesis during murine embryonic development [ 12 ], and Dengue virus infection proved to inhibit SA in vitro [ 13 ].…”

Section: Angiogenesis and Viral Infectionsmentioning

confidence: 99%

Intussusceptive angiogenesis in Covid-19: hypothesis on the significance and focus on the possible role of FGF2

2020

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The interest on the role of angiogenesis in the pathogenesis and progression of human interstitial lung diseases is growing, with conventional sprouting (SA) and non-sprouting intussusceptive angiogenesis (IA) being differently represented in specific pulmonary injury patterns. The role of viruses as key regulators of angiogenesis is known for several years. A significantly enhanced amount of new vessel growth, through a mechanism of IA, has been reported in lungs of patients who died from Covid-19; among the angiogenesis-related genes, fibroblast growth factor 2 (FGF2) was found to be upregulated. These findings are intriguing. FGF2 plays a role in some viral infections: the upregulation is involved in the MERS-CoV-induced strong apoptotic response crucial for its highly lytic replication cycle in lung cells, whereas FGF2 is protective against the acute lung injury induced by H1N1 influenza virus, improving the lung wet-to-dry weight ratio. FGF2 plays a role also in regulating IA, acting on pericytes (crucial for the formation of intraluminal pillars), and endothelium, and FGF2-induced angiogenesis may be promoted by inflammation and hypoxia. IA is a faster and probably more efficient process than SA, able to modulate vascular remodeling through pruning of redundant or inefficient blood vessels. We can speculate that IA might have the function of restoring a functional vascular plexus consequently to extensive endothelialitis and alveolar capillary micro-thrombosis observed in Covid-19. Anti-Vascular endothelial growth factor (anti-VEGF) strategies are currently investigated for treatment of severe and critically ill Covid-19 patients, but also FGF2, and its expression and/or signaling, might represent a promising target.

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Parvovirus B19-induced angiogenesis in fulminant myocarditis

Cited by 23 publications

References 0 publications

Inflammation and intussusceptive angiogenesis in COVID-19: everything in and out of flow

Inflammation and intussusceptive angiogenesis in COVID-19: everything in and out of flow

Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes

Intussusceptive angiogenesis in Covid-19: hypothesis on the significance and focus on the possible role of FGF2

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