Tsantan Sumtang attenuated chronic hypoxia-induced right ventricular structure remodeling and fibrosis by equilibrating local ACE-AngII-AT1R/ACE2-Ang1-7-Mas axis in rat

Dang, Zhancui; Su, Shanshan; Jin, Guoen; Nan, Xingmei; Ma, Lan; Li, Zhanqiang; Lu, Dianxiang; Ge, Ri‐Li

doi:10.1016/j.jep.2019.112470

Cited by 69 publications

(52 citation statements)

References 48 publications

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“…Zhang et al (2009) reported a blunted expression of ACE-2 in cell lines exposed to severe hypoxia (2% oxygen) over 12 days. A similar observation was made by Dang et al (2020) when rats were exposed to the hypoxia equivalent of *4500 m altitude over 45 days.…”

Section: Hypoxiasupporting

confidence: 76%

Lower Incidence of COVID-19 at High Altitude: Facts and Confounders

Pun

Turner

Strapazzon

et al. 2020

High Altitude Medicine & Biology

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The rapid transmission, increased morbidity, and mortality of coronavirus disease 2019 (COVID-19) has exhausted many health care systems and the global economy. Large variations in COVID-19 prevalence and incidence have been reported across and within many countries worldwide; however, this remains poorly understood. The variability and susceptibility across the world have been mainly attributed to differing socioeconomic status, burden of chronic diseases, access to health care, strength of health care systems, and early or late adoption of control measures. Environmental factors such as pollution, ambient temperature, humidity, and seasonal weather patterns at different latitudes may influence how severe the pandemic is and the incidence of infection in any part of the world. In addition, recent epidemiological data have been used to propose that altitude of residence may not only influence those environmental features considered key to lesser viral transmission, but also susceptibility to more severe forms of COVID-19 through hypoxic-hypobaria driven genomic or nongenomic adaptations specific to high-altitude populations. In this review, we critically examine these factors and attempt to determine based upon available scientific and epidemiological data whether living in high-altitude regions might be protective against COVID-19 as recent publications have claimed.

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Section: Hypoxiasupporting

confidence: 76%

Lower Incidence of COVID-19 at High Altitude: Facts and Confounders

Pun

Turner

Strapazzon

et al. 2020

High Altitude Medicine & Biology

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“…However, under chronic hypoxia (O2 2% for 12 days) ACE1 is upregulated by the hypoxia-inducible factor 1 (HIF-1) (a master regulator of the response to hypoxia) in human pulmonary artery smooth muscle cells (hPASMC), while the expression of ACE2 is markedly decreased (Zhang et al 2009). Similar results were obtained in rats (males, SD) exposed to conditions equivalent to 4,500 meters of altitude, which after 28 days showed increased levels of ACE1 and decreased expression of ACE2 in heart cells (Dang et al 2020). These observations are highly relevant for the pathogenesis of COVID-19, since the level of expression of ACE2 in pulmonary epithelial cells has been demonstrated to be positively correlated with the rate of infection of the first SARS-CoV (Jia et al 2005;Lu et al 2020;Ren et al 2020;Rothan and Byrareddy 2020).…”

Section: Introductionsupporting

confidence: 81%

Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?

Arias‐Reyes

Zubieta-DeUrioste

Poma-Machicao

et al. 2020

Respiratory Physiology & Neurobiology

204

224

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Does the pathogenesis of SAR-CoV-2 virus decrease at high-altitude?, Respiratory Physiology and amp; Neurobiology (2020), doi: https://doi. J o u r n a l P r e -p r o o fHighlights  COVID-19 infection is decreased in populations living at an altitude of above 3,000 masl  Highland inhabitants may be less susceptible to SARS-CoV-2 virus infection due to physiological acclimatization to hypoxia  High-altitude environmental factors may contribute to reduce the virulence of SARS-CoV-2 ABSTRACTIn the present study we analyze the epidemiologic data of COVID-19 of Tibet and high-altitude regions of Bolivia and Ecuador, and compare to lowland data, to test the hypothesis that high-altitude inhabitants (+2500 m above sea-level) are less susceptible to develop severe adverse effect in acute SARS-CoV-2 virus infection. Analysis of available epidemiological data suggest that physiological adaptations that counterbalance the hypoxic environment altitude may protect from severe impact of acute SARS-CoV-2 virus infection. Potential underlying mechanisms such as: (i) a compromised half-live of the virus caused by the high-altitude environment, and (ii) a hypoxia mediated down regulation of angiotensin-converting enzyme 2 (ACE2), which is the main binding target of SARS-CoV-2 virus in the pulmonary epithelia are discussed.

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“…Supporting the role of fibrosis, a recent study in rats with RVH induced by hypobaric hypoxia (4500 m) exposure showed a fibrotic process in the RV [89]. A study in mice under other types of hypoxia (chronic normobaric hypoxia, 10% O 2 ) showed that animals with PO-induced RVH and HF exhibited increased p38α expression, which was related to several effects, such as increased collagen and smooth muscle actin α (α-SMA) content leading to fibrosis [90].…”

Section: Fibrosismentioning

confidence: 88%

Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

Peña

Brito

Alam

et al. 2020

IJMS

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High altitude (hypobaric hypoxia) triggers several mechanisms to compensate for the decrease in oxygen bioavailability. One of them is pulmonary artery vasoconstriction and its subsequent pulmonary arterial remodeling. These changes can lead to pulmonary hypertension and the development of right ventricular hypertrophy (RVH), right heart failure (RHF) and, ultimately to death. The aim of this review is to describe the most recent molecular pathways involved in the above conditions under this type of hypobaric hypoxia, including oxidative stress, inflammation, protein kinases activation and fibrosis, and the current therapeutic approaches for these conditions. This review also includes the current knowledge of long-term chronic intermittent hypobaric hypoxia. Furthermore, this review highlights the signaling pathways related to oxidative stress (Nox-derived O2.- and H2O2), protein kinase (ERK5, p38α and PKCα) activation, inflammatory molecules (IL-1β, IL-6, TNF-α and NF-kB) and hypoxia condition (HIF-1α). On the other hand, recent therapeutic approaches have focused on abolishing hypoxia-induced RVH and RHF via attenuation of oxidative stress and inflammatory (IL-1β, MCP-1, SDF-1 and CXCR-4) pathways through phytotherapy and pharmacological trials. Nevertheless, further studies are necessary.

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Tsantan Sumtang attenuated chronic hypoxia-induced right ventricular structure remodeling and fibrosis by equilibrating local ACE-AngII-AT1R/ACE2-Ang1-7-Mas axis in rat

Cited by 69 publications

References 48 publications

Lower Incidence of COVID-19 at High Altitude: Facts and Confounders

Lower Incidence of COVID-19 at High Altitude: Facts and Confounders

Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?

Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

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