Hypoxia Signaling in Cardiovascular Diseases

Gupta, Neha; Ashraf, Mohammad Zahid

doi:10.5772/intechopen.80456

Cited by 7 publications

(6 citation statements)

References 90 publications

(91 reference statements)

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“…NF-κB signaling pathway promotes inflammation by inducing expression of pro-inflammatory cytokines. It has been shown that IH plays a role in OSA pathogenesis and cardiovascular complications through activation of pro-inflammatory pathways [ 6 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

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Obstructive Sleep Apnea Syndrome In Vitro Model: Controlled Intermittent Hypoxia Stimulation of Human Stem Cells-Derived Cardiomyocytes

Regev

Etzion

Haddad

et al. 2022

IJMS

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Cardiovascular morbidity is the leading cause of death of obstructive sleep apnea (OSA) syndrome patients. Nocturnal airway obstruction is associated with intermittent hypoxia (IH). In our previous work with cell lines, incubation with sera from OSA patients induced changes in cell morphology, NF-κB activation and decreased viability. A decrease in beating rate, contraction amplitude and a reduction in intracellular calcium signaling was also observed in human cardiomyocytes differentiated from human embryonic stem cells (hESC-CMs). We expanded these observations using a new controlled IH in vitro system on beating hESC-CMs. The Oxy-Cycler system was programed to generate IH cycles. Following IH, we detected the activation of Hif-1α as an indicator of hypoxia and nuclear NF-κB p65 and p50 subunits, representing pro-inflammatory activity. We also detected the secretion of inflammatory cytokines, such as MIF, PAI-1, MCP-1 and CXCL1, and demonstrated a decrease in beating rate of hESC-CMs following IH. IH induces the co-activation of inflammatory features together with cardiomyocyte alterations which are consistent with myocardial damage in OSA. This study provides an innovative approach for in vitro studies of OSA cardiovascular morbidity and supports the search for new pharmacological agents and molecular targets to improve diagnosis and treatment of patients.

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Section: Discussionmentioning

confidence: 99%

“…HIF-1 (hypoxia inducible factor-1) is a transcription factor that has a key role in cell adaption to hypoxic conditions [ 6 ]. In normoxic conditions, the Hif-1α subunit is ubiquitinated and degraded by the proteosome.…”

Section: Introductionmentioning

confidence: 99%

Obstructive Sleep Apnea Syndrome In Vitro Model: Controlled Intermittent Hypoxia Stimulation of Human Stem Cells-Derived Cardiomyocytes

Regev

Etzion

Haddad

et al. 2022

IJMS

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“…Chronic and acute hypoxic exposure has been shown to trigger endothelial damage and vascular inflammation (Tarbell et al, 2020), increasing an individual's risk of vascular injury that can lead to adverse outcomes, such as cardiovascular disease (Lee et al, 2019). Moreover, the progressive nature of cardiovascular disease is also proposed to exacerbate vascular hypoxia (Gupta & Zahid Ashraf, 2018), resulting in a reciprocal cycle. The endothelium plays a pivotal role in this cycle; therefore, it is important to understand the deleterious effects of hypo-…”

Section: Introductionmentioning

confidence: 99%

The deleterious effects of acute hypoxia on microvascular and large vessel endothelial function

Jones

Macdonald

Sandoo

et al. 2021

Experimental Physiology

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Hypoxia is associated with diminished bioavailability of the endothelium-derived vasodilator, nitric oxide (NO). Diminished NO bioavailability can have deleterious effects on endothelial function. The endothelium is a heterogeneous tissue; therefore, a comprehensive assessment of endothelial function is crucial to understand the significance of hypoxia-induced endothelial dysfunction. We hypothesized that acute hypoxia would have a deleterious effect on microvascular and large vessel endothelial function. Twenty-nine healthy adults [24 (SD = 4 ) years of age] completed normoxic and hypoxic [inspired O 2 fraction = 0.209] trials in this double-blinded, counterbalanced crossover study. After 30 min, we assessed the laser Doppler imaging-determined perfusion response to iontophoresis of ACh as a measure of endothelium-dependent microvascular function and iontophoresis of sodium nitroprusside as a measure of endothelium-independent microvascular function. After 60 min, we assessed brachial flow-mediated dilatation as a measure of large vessel K E Y W O R D S cardiorespiratory fitness, endothelium, iontophoresis, nitric oxide, vasodilatationThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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“…ROS cause lipid peroxidation, endothelial injury, increased vascular permeability, and disruption of BBB, which may further enhance the tissue edema ( 161 ). HIF-1 and ROS are involved in the pathogenesis, progression, and rupture of atherosclerotic plaques and arterial thrombosis ( 162 ).…”

Section: Hypoxiamentioning

confidence: 99%

Stroke in SARS-CoV-2 Infection: A Pictorial Overview of the Pathoetiology

Neshin

Shahjouei

Koza

et al. 2021

Front. Cardiovasc. Med.

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Since the early days of the pandemic, there have been several reports of cerebrovascular complications during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Numerous studies proposed a role for SARS-CoV-2 in igniting stroke. In this review, we focused on the pathoetiology of stroke among the infected patients. We pictured the results of the SARS-CoV-2 invasion to the central nervous system (CNS) via neuronal and hematogenous routes, in addition to viral infection in peripheral tissues with extensive crosstalk with the CNS. SARS-CoV-2 infection results in pro-inflammatory cytokine and chemokine release and activation of the immune system, COVID-19-associated coagulopathy, endotheliitis and vasculitis, hypoxia, imbalance in the renin-angiotensin system, and cardiovascular complications that all may lead to the incidence of stroke. Critically ill patients, those with pre-existing comorbidities and patients taking certain medications, such as drugs with elevated risk for arrhythmia or thrombophilia, are more susceptible to a stroke after SARS-CoV-2 infection. By providing a pictorial narrative review, we illustrated these associations in detail to broaden the scope of our understanding of stroke in SARS-CoV-2-infected patients. We also discussed the role of antiplatelets and anticoagulants for stroke prevention and the need for a personalized approach among patients with SARS-CoV-2 infection.

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Hypoxia Signaling in Cardiovascular Diseases

Cited by 7 publications

References 90 publications

Obstructive Sleep Apnea Syndrome In Vitro Model: Controlled Intermittent Hypoxia Stimulation of Human Stem Cells-Derived Cardiomyocytes

Obstructive Sleep Apnea Syndrome In Vitro Model: Controlled Intermittent Hypoxia Stimulation of Human Stem Cells-Derived Cardiomyocytes

The deleterious effects of acute hypoxia on microvascular and large vessel endothelial function

Stroke in SARS-CoV-2 Infection: A Pictorial Overview of the Pathoetiology

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