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

Peña, Emilio Duro; Brito, Julio; Alam, Samia El; Siqués, Patricia

doi:10.3390/ijms21176421

Cited by 78 publications

(47 citation statements)

References 115 publications

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“…Under hypoxic conditions, the activity of HIF-1α is closely related to inflammation. 71 It regulates the secretion of cytokines, the differentiation of monocytes into macrophages accompanied by the secretion of cytokines such as IL-1β, IL-6, IL-12, IL-23 and TNF-α. [72][73][74] It is important to note that HIF-1α may be stabilized by inflammatory cytokines, especially TNF-α, inducing positive feedback, stimulating further differentiation of monocytes into macrophage.…”

Section: Discussionmentioning

confidence: 99%

Cross-Talk Between Nitrosative Stress, Inflammation and Hypoxia-Inducible Factor in Patients with Adrenal Masses

Choromańska¹,

Myśliwiec²,

Kozłowski³

et al. 2021

JIR

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Background: Adrenal masses are the most common of all human tumors. The role of nitrosative stress and inflammation in cancer development has already been demonstrated. However, it is not known whether they are involved in the pathogenesis of adrenal tumors. The aim of the study was to investigate a cross-talk between nitrosative stress, inflammation and hypoxia-inducible factor (HIF-1α) in 75 patients with different types of adrenal masses (non-functional incidentaloma, pheochromocytoma and Cushing's/Conn's adenoma). Methods: The plasma concentrations of total nitric oxide (NO), S-nitrosothiols, peroxynitrite nitrotyrosine and the activity of serum myeloperoxidase (MPO) were measured spectrophotometrically, whereas concentrations of interleukin 1 beta (IL-1β), tumor necrosis factor α (TNF-α) and hypoxia-inducible factor 1 alpha (HIF-1α) were measured using commercial ELISA kits. The control group consisted of 50 healthy people matched by age and sex to the study group. The number of subjects was determined a priori based on our previous experiment (power of the test = 0.9; α = 0.05). Results: We found significantly higher nitrosative stress (↑nitric oxide, ↑peroxynitrite, ↑S-nitrosothiols and ↑nitrotyrosine) in the plasma of patients with adrenal tumors, which was accompanied by increased inflammatory (↑myeloperoxidase, ↑interleukin 1 beta and ↑tumor necrosis factor α) and hypoxia (HIF-1α) biomarkers. Peroxynitrite and nitrotyrosine were positively correlated with aldosterone level. Nitrosative stress was also associated with inflammation and HIF-1α. Interestingly, plasma nitrotyrosine and serum MPO differentiated patients with adrenal tumor from healthy individuals with high sensitivity and specificity. Moreover, using multivariate regression analysis, we showed that ONOO − and IL-1β depended on cortisol level, while ONOO − , nitrotyrosine and HIF-1α were associated with aldosterone. Unfortunately, none of the assessed biomarkers differentiated between tumor types studied, suggesting that the severity of nitrosative damage and inflammation are similar in patients with incidentaloma, pheochromocytoma, and Cushing's or Conn's adenoma. Conclusion: Adrenal tumors are associated with increased protein nitration/S-nitrosylation and inflammation.

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Section: Discussionmentioning

confidence: 99%

Cross-Talk Between Nitrosative Stress, Inflammation and Hypoxia-Inducible Factor in Patients with Adrenal Masses

Choromańska¹,

Myśliwiec²,

Kozłowski³

et al. 2021

JIR

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“…Repeated hypoxia-reoxygenation in OSAS leads to ED through oxidative stress, inflammation, and sympathetic nerve activation among many other pathological reactions involved in disease occurrence (Prabhakar et al, 2020). Recently, a new condition associated with high altitude (i.e., long-term chronic IH) was reported in South America (Pena et al, 2020). Long-term chronic IH afflicts people that commute to work at high altitudes but live and rest at sea level.…”

Section: Chronic Ih and Vascular Ed Chronic Ihmentioning

confidence: 99%

Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction

Yanli

Wang

et al. 2021

Front. Physiol.

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Endothelial dysfunction (ED) is a core pathophysiological process. The abnormal response of vascular endothelial (VE) cells to risk factors can lead to systemic consequences. ED caused by intermittent hypoxia (IH) has also been recognized. Neuropeptide Y (NPY) is an important peripheral neurotransmitter that binds to different receptors on endothelial cells, thereby causing ED. Additionally, hypoxia can induce the release of peripheral NPY; however, the involvement of NPY and its receptor in IH-induced ED has not been determined. This review explains the definition of chronic IH and VE function, including the relationship between ED and chronic IH-related vascular diseases. The results showed that that the effect of IH on VE injury is mediated by the VE-barrier structure and endothelial cell dysfunction. These findings offer new ideas for the prevention and treatment of obstructive sleep apnea syndrome and its complications.

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“…In cardiovascular cells ROS is continuously produced by NADPH oxidase. Angiotensin II, TNF-α, cyclic stretch and endothelin-1 are the different stimuli that enhanced the activity of ROS (Pena, Brito, El Alam, & Siques, 2020…”

Section: Oxidative Stressmentioning

confidence: 99%

Analyzing and Identifying the Molecular Targets and Regulators Controlling Cardiac Hypertrophy Progression

Shad

Shah

Zulqarnain

et al. 2021

NJNS

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Cardiac hypertrophy is the major pathway by which neurohormonal and mechanical stimuli act upon cardiomyocytes which gives the response to these stimuli. It leads to heart failure and ventricular dilation which is the main root of mortality in the western world. Many molecular targets are controlling cardiac hypertrophy development which may influence the growth factors signaling, cytokine release and gene expression. Through clinical trials on different models, recent research shows that cardiac hypertrophy might be inhibited or reversed. These findings have developed a vast drive to recognize specific and novel regulators of cardiac hypertrophy. Many molecular targets and signaling modulators have been studied in this review that induce the hypertrophic response which may involve MAPK pathway, oxidative stress, calcineurin, Cardiac angiogenesis, serum protein concentration, microRNA, and periodontitis. For the treatment of cardiac hypertrophy, the scientific knowledge of these signaling pathways and factors may be translated into potential nutritional and molecular therapies for the betterment of this diseases. The current and previous knowledge of molecular markers can be compiled in this review for the treatment of the molecular pathogenesis of cardiac hypertrophy.

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

Cited by 78 publications

References 115 publications

Cross-Talk Between Nitrosative Stress, Inflammation and Hypoxia-Inducible Factor in Patients with Adrenal Masses

Cross-Talk Between Nitrosative Stress, Inflammation and Hypoxia-Inducible Factor in Patients with Adrenal Masses

Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction

Analyzing and Identifying the Molecular Targets and Regulators Controlling Cardiac Hypertrophy Progression

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