Pulmonary hypertension: the hallmark of acute COVID-19 microvascular angiopathy?

Dintakurti, Sri Harsha; Kamath, Sanjana; Mahon, Caroline; Singh, Suveer; Rawal, Bhavin; Padley, Simon; Devaraj, Anand; Price, Laura; Desai, Sujal R.; Semple, Thomas; Ridge, Carole A.

doi:10.1183/23120541.00389-2022

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…A very important finding emerged from the study of Dintakurti et al, 27 who investigated the incidence of in situ pulmonary thrombosis in patients with COVID-19 ( n = 25) or influenza ( n = 25) pneumonia. Overall, the incidence of pulmonary arterial thrombosis was 60% in patients with COVID-19 and 44% in those with influenza ( p = 0.40), but the observation of isolate pulmonary arterial thrombi (which reflects in situ pulmonary thrombosis) was remarkably high in both categories of patients, being 44% in COVID-19 patients and 32% in those with influenza ( p = 0.56).…”

Section: Thrombotic Potency Of Sars-cov-2 and Influenza Virusesmentioning

confidence: 99%

Venous Thrombosis in Airborne Viral Infections: Is Coronavirus Disease 2019 now Any Different from Influenza?

Lippi,

Favaloro,

Nocini

2024

Semin Thromb Hemost

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One of the hallmarks of coronavirus disease 2019 (COVID-19), particularly in complicated cases (i.e., requiring hospitalization or intensive care support), is persistent hemostasis activation, which may be associated with a vast array of thrombotic episodes involving both the arterial and venous systems. The renewed emphasis on the relationship between viral infections and venous thrombosis paves the way for determining whether a more common and often underestimated infection disease, such as influenza, may also be associated with a significant burden of venous thrombotic episodes, and how this eventual thrombotic risk compares to that seen in COVID-19, both in the past and with newer variants. Our review of studies comparing the burden of venous thromboembolism (VTE) in patients with COVID-19 or influenza revealed that the thrombotic risk appears to be significantly higher in patients with COVID-19 but remains certainly not meaningless in those with influenza, particularly in subjects infected by highly virulent strains (i.e., H1N1), in those who develop pneumonia and require intensive care support. In these specific clinical settings, the adoption of tailored thromboprophylaxis may be indicated though more studies are compellingly needed on this matter. As COVID-19 variants emerge, there is a possibility that the VTE burden of COVID-19 will decrease, and progress to that of other respiratory viruses.

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Section: Thrombotic Potency Of Sars-cov-2 and Influenza Virusesmentioning

confidence: 99%

Venous Thrombosis in Airborne Viral Infections: Is Coronavirus Disease 2019 now Any Different from Influenza?

Lippi,

Favaloro,

Nocini

2024

Semin Thromb Hemost

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“…Studies have reported on the pulmonary hypertension (PH) occurrence and development in population infected by SARS-CoV-2 or with COVID-19. [17][18][19][20][21][22] Upon SARS-CoV-2 infection, the predicted PH prevalence is supposed to be 12% 23 and 39% 24 in patients of non-intensive care unit (ICU) and ICU population, respectively. These clinical findings suggest the association among SARS-CoV-2, developmental pulmonary vascular damage and the occurrence of PH.…”

Section: Introductionmentioning

confidence: 99%

SARS-CoV-2 spike protein receptor-binding domain perturbates intracellular calcium homeostasis and impairs pulmonary vascular endothelial cells

Yang

Liu

Han

et al. 2023

Sig Transduct Target Ther

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Exposure to the spike protein or receptor-binding domain (S-RBD) of SARS-CoV-2 significantly influences endothelial cells and induces pulmonary vascular endotheliopathy. In this study, angiotensin-converting enzyme 2 humanized inbred (hACE2 Tg) mice and cultured pulmonary vascular endothelial cells were used to investigate how spike protein/S-RBD impacts pulmonary vascular endothelium. Results show that S-RBD leads to acute-to-prolonged induction of the intracellular free calcium concentration ([Ca2+]i) via acute activation of TRPV4, and prolonged upregulation of mechanosensitive channel Piezo1 and store-operated calcium channel (SOCC) key component Orai1 in cultured human pulmonary arterial endothelial cells (PAECs). In mechanism, S-RBD interacts with ACE2 to induce formation of clusters involving Orai1, Piezo1 and TRPC1, facilitate the channel activation of Piezo1 and SOCC, and lead to elevated apoptosis. These effects are blocked by Kobophenol A, which inhibits the binding between S-RBD and ACE2, or intracellular calcium chelator, BAPTA-AM. Blockade of Piezo1 and SOCC by GsMTx4 effectively protects the S-RBD-induced pulmonary microvascular endothelial damage in hACE2 Tg mice via normalizing the elevated [Ca2+]i. Comparing to prototypic strain, Omicron variants (BA.5.2 and XBB) of S-RBD induces significantly less severe cell apoptosis. Transcriptomic analysis indicates that prototypic S-RBD confers more severe acute impacts than Delta or Lambda S-RBD. In summary, this study provides compelling evidence that S-RBD could induce persistent pulmonary vascular endothelial damage by binding to ACE2 and triggering [Ca2+]i through upregulation of Piezo1 and Orai1. Targeted inhibition of ACE2-Piezo1/SOCC-[Ca2+]i axis proves a powerful strategy to treat S-RBD-induced pulmonary vascular diseases.

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“…Pulmonary hypertension (PH) is a rare but serious condition in which there is increased pressure in the blood vessels of the lungs, which can lead to heart failure and death. PH can be caused by a variety of underlying conditions, such as lung disease, heart disease, or genetic factors [1][2][3]. One specific subtype of PH is called pulmonary hypertension due to hypoxia, which is characterised by increased resistance in the small arteries of the lungs [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of pulmonary artery smooth muscle cells via the delivery of curcuminoid WZ35 by Cu‐based metal organic frameworks

Hua

Han

Song

et al. 2023

IET Nanobiotechnology

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Hypoxic pulmonary hypertension (HPH) is a life‐threatening disease that occurs due to a lack of oxygen in the lungs, leading to an increase in pulmonary vascular resistance, right ventricular failure, and ultimately death. HPH is a multifactorial disorder that involves multiple molecular pathways, making it a challenge for clinicians to identify effective therapies. Pulmonary artery smooth muscle cells (PASMCs) play a crucial role in HPH pathogenesis by proliferating, resisting apoptosis, and promoting vascular remodelling. Curcumin, a natural polyphenolic compound, has shown potential as a therapeutic agent for HPH by reducing pulmonary vascular resistance, inhibiting vascular remodelling, and promoting apoptosis of PASMCs. Regulation of PASMCs could significantly inhibits HPH. However, curcumin has the disadvantages of poor solubility and low bioavailability, and its derivative WZ35 has better biosafety. Here, Cu‐based metal organic frameworks (MOFCu) was fabricated to encapsulate the curcumin analogue WZ35 (MOFCu@WZ35) for the inhibition of PASMCs proliferation. The authors found that the MOFCu@WZ35 could promote the death of PASMCs. Furthermore, the authors believed that this drug delivery system will effectively alleviate the HPH.

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Pulmonary hypertension: the hallmark of acute COVID-19 microvascular angiopathy?

Cited by 4 publications

References 13 publications

Venous Thrombosis in Airborne Viral Infections: Is Coronavirus Disease 2019 now Any Different from Influenza?

Venous Thrombosis in Airborne Viral Infections: Is Coronavirus Disease 2019 now Any Different from Influenza?

SARS-CoV-2 spike protein receptor-binding domain perturbates intracellular calcium homeostasis and impairs pulmonary vascular endothelial cells

Inhibition of pulmonary artery smooth muscle cells via the delivery of curcuminoid WZ35 by Cu‐based metal organic frameworks

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