Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation

Pulmonary arterial hypertension (PAH) is a pulmonary vascular disease characterized by the progressive elevation of pulmonary arterial pressures. It is becoming increasingly apparent that inflammation contributes to the pathogenesis and progression of PAH. Several viruses are known to cause PAH, suc...

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Main Authors: Desheng Wang, Marta T. Gomes, Yanfei Mo, Clare C. Prohaska, Lu Zhang, Sarvesh Chelvanambi, Matthias A. Clauss, Dongfang Zhang, Roberto F. Machado, Mingqi Gao, Yang Bai
Format: Article
Language:English
Published: MDPI AG 2023-04-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/24/8/7472
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author Desheng Wang
Marta T. Gomes
Yanfei Mo
Clare C. Prohaska
Lu Zhang
Sarvesh Chelvanambi
Matthias A. Clauss
Dongfang Zhang
Roberto F. Machado
Mingqi Gao
Yang Bai
author_facet Desheng Wang
Marta T. Gomes
Yanfei Mo
Clare C. Prohaska
Lu Zhang
Sarvesh Chelvanambi
Matthias A. Clauss
Dongfang Zhang
Roberto F. Machado
Mingqi Gao
Yang Bai
author_sort Desheng Wang
collection DOAJ
description Pulmonary arterial hypertension (PAH) is a pulmonary vascular disease characterized by the progressive elevation of pulmonary arterial pressures. It is becoming increasingly apparent that inflammation contributes to the pathogenesis and progression of PAH. Several viruses are known to cause PAH, such as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), human endogenous retrovirus K(HERV-K), and human immunodeficiency virus (HIV), in part due to acute and chronic inflammation. In this review, we discuss the connections between HERV-K, HIV, SARS-CoV-2, and PAH, to stimulate research regarding new therapeutic options and provide new targets for the treatment of the disease.
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spelling doaj.art-c72ca65734a449cca5cf2dff814202022023-11-17T19:40:57ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-04-01248747210.3390/ijms24087472Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth StimulationDesheng Wang0Marta T. Gomes1Yanfei Mo2Clare C. Prohaska3Lu Zhang4Sarvesh Chelvanambi5Matthias A. Clauss6Dongfang Zhang7Roberto F. Machado8Mingqi Gao9Yang Bai10Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, ChinaDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN 46202, USADepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, ChinaDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN 46202, USADepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, ChinaDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN 46202, USADivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN 46202, USADepartment of Pharmacognosy, School of Pharmacy, China Medical University, Shenyang 110122, ChinaDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN 46202, USADepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, ChinaDepartment of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang 110122, ChinaPulmonary arterial hypertension (PAH) is a pulmonary vascular disease characterized by the progressive elevation of pulmonary arterial pressures. It is becoming increasingly apparent that inflammation contributes to the pathogenesis and progression of PAH. Several viruses are known to cause PAH, such as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), human endogenous retrovirus K(HERV-K), and human immunodeficiency virus (HIV), in part due to acute and chronic inflammation. In this review, we discuss the connections between HERV-K, HIV, SARS-CoV-2, and PAH, to stimulate research regarding new therapeutic options and provide new targets for the treatment of the disease.https://www.mdpi.com/1422-0067/24/8/7472human endogenous retrovirus Kpulmonary arterial hypertensionhuman immunodeficiency virusSARS-CoV-2inflammation
spellingShingle Desheng Wang
Marta T. Gomes
Yanfei Mo
Clare C. Prohaska
Lu Zhang
Sarvesh Chelvanambi
Matthias A. Clauss
Dongfang Zhang
Roberto F. Machado
Mingqi Gao
Yang Bai
Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation
International Journal of Molecular Sciences
human endogenous retrovirus K
pulmonary arterial hypertension
human immunodeficiency virus
SARS-CoV-2
inflammation
title Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation
title_full Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation
title_fullStr Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation
title_full_unstemmed Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation
title_short Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation
title_sort human endogenous retrovirus sars cov 2 and hiv promote pah via inflammation and growth stimulation
topic human endogenous retrovirus K
pulmonary arterial hypertension
human immunodeficiency virus
SARS-CoV-2
inflammation
url https://www.mdpi.com/1422-0067/24/8/7472
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