Ventilatory and Autonomic Regulation in Sleep Apnea Syndrome: A Potential Protective Role for Erythropoietin?

Andrade, David C.; Haine, Liasmine; Toledo, Camilo; Díaz, Hugo S.; Quintanilla, Rodrigo A.; Marcus, Noah J.; Iturriaga, Rodrigo; Richalet, Jean‐Paul; Voituron, Nicolas; Rio, Rodrigo Del

doi:10.3389/fphys.2018.01440

Cited by 11 publications

(11 citation statements)

References 99 publications

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“…There are emerging evidences for the neuroprotection effect of EPO both in vivo and in vitro [21,38,39]. The positive roles that EPO may play in APAC under higher dose, such as anti-apoptotic [12,13], anti-oxidant [14], and antiin ammatory [15,16] make it an ideal treatment in APAC. However, its role in angiogenesis, causing neovascularization is a dreaded occurrence in the eye [40].…”

Section: Discussionmentioning

confidence: 99%

“…However, there has been no research describing the changes of EPO and PDGF levels in APAC eyes. Recent studies have shown that both EPO and PDGF have neuroprotective functions such as anti-apoptotic [12,13], anti-oxidant [14] and anti-in ammatory properties [15,16]. Thus, the uctuations of their levels in aqueous humor may correlate with prognosis of trabeculectomy in APAC eyes.…”

Section: Introductionmentioning

confidence: 99%

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Potential Effects of Angiogenesis-related Factors on the Severity of APAC and Surgical Outcomes of Trabeculectomy

Wang

Zhou

et al. 2020

Preprint

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Background. Acute primary angle closure (APAC) caused by an abrupt closure of trabecular meshwork can develop into angle closure glaucoma due to uncontrolled IOP. Under reduced oxygen tension, hypoxia inducible transcription factors will be accumulated. EPO (erythropoietin) and PDGF (platelet derived growth factor) families are thought to be associated with angiogenesis under hypoxic condition.Methods. Concentrations of EPO, PDGF-AA, -BB, -CC and -DD collected in aqueous humor samples were measured. Before operations, correlations between target proteins and IOP were detected between APAC (acute primary angle closure) and cataract patients. Based on the post-operative follow-up, the effects of EPO and PDGF family members on the successful rate of trabeculectomy were tested. Results. The levels of EPO, PDGF-CC and -DD were significantly elevated in the APAC group compared to the cataract group. During the post-operative follow-up, EPO, PDGF-CC and -DD showed significant differences between the success and failure groups. In multivariable linear regression analyses, failed filtration surgery was more likely in APAC eyes with higher EPO level. The Kaplan-Meier survival plot suggested that the success rate in eyes with low EPO level was significantly higher than that in eyes with high EPO level.Conclusion. The levels of EPO, PDGF-CC and -DD were significantly elevated in failure group. EPO level correlated with preoperative IOP and numbers of eyedrops, and higher EPO level in aqueous humor is a risk factor for trabeculectomy failure. It can be a biomarker to estimate the severity of APAC and the success rate of surgery. The investigation of mechanism of EPO in APAC a may have potential clinical applications for the surgical treatment of APAC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potential Effects of Angiogenesis-related Factors on the Severity of APAC and Surgical Outcomes of Trabeculectomy

Wang

Zhou

et al. 2020

Preprint

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“…Its target receptors are expressed in several cell types including skeletal muscle [42][43][44][45][46][47][48][49]. EPO has a tissue protective potential, including anti-inflammation, anti-apoptosis, and improving metabolic alteration [48,[50][51][52][53]. EPO reduced cells apoptosis and inhibited pro-inflammatory cytokines in sepsis-induced lung injury model [54] as well as in kidney ischemia/ reperfusion injury model [55].…”

Section: Ivyspringmentioning

confidence: 99%

Erythropoietin Alleviates Burn-induced Muscle Wasting

Tai

et al. 2020

Int. J. Med. Sci.

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Background: Burn injury induces long-term skeletal muscle pathology. We hypothesized EPO could attenuate burn-induced muscle fiber atrophy. Methods: Rats were allocated into four groups: a sham burn group, an untreated burn group subjected to third degree hind paw burn, and two burn groups treated with weekly or daily EPO for four weeks. Gastrocnemius muscle was analyzed at four weeks post-burn. Results: EPO attenuated the reduction of mean myofiber cross-sectional area post-burn and the level of the protective effect was no significant difference between two EPO-treated groups (p=0.784). Furthermore, EPO decreased the expression of atrophy-related ubiquitin ligase, atrogin-1, which was up-regulated in response to burn. Compared to untreated burn rats, those receiving weekly or daily EPO groups had less cell apoptosis by TUNEL assay. EPO decreased the expression of cleaved caspase 3 (key factor in the caspase-dependent pathway) and apoptosis-inducing factor (implicated in the caspase-independent pathway) after burn. Furthermore, EPO alleviated connective tissue overproduction following burn via transforming growth factor beta 1-Smad2/3 pathway. Daily EPO group caused significant erythrocytosis compared with untreated burn group but not weekly EPO group. Conclusion: EPO therapy attenuated skeletal muscle apoptosis and fibrosis at four weeks post-burn. Weekly EPO may be a safe and effective option in muscle wasting post-burn.

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“…They are composed of type I glomus cells and type II glial cells. Type I cells respond to an impairment in blood flow and mainly to decreasing levels of arterial PO 2 (Andrade et al, 2018). The carotid body chemoreflex modulates sympathetic drive to the heart and vasculature to maintain blood pressure.…”

Section: Mechanisms Of Cih-induced Hypertensionmentioning

confidence: 99%

Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension?

2019

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Renal sensory nerves are important in the regulation of body fluid and electrolyte homeostasis, and blood pressure. Activation of renal mechanoreceptor afferents triggers a negative feedback reno-renal reflex that leads to the inhibition of sympathetic nervous outflow. Conversely, activation of renal chemoreceptor afferents elicits reflex sympathoexcitation. Dysregulation of reno-renal reflexes by suppression of the inhibitory reflex and/or activation of the excitatory reflex impairs blood pressure control, predisposing to hypertension. Obstructive sleep apnoea syndrome (OSAS) is causally related to hypertension. Renal denervation in patients with OSAS or in experimental models of chronic intermittent hypoxia (CIH), a cardinal feature of OSAS due to recurrent apnoeas (pauses in breathing), results in a decrease in circulating norepinephrine levels and attenuation of hypertension. The mechanism of the beneficial effect of renal denervation on blood pressure control in models of CIH and OSAS is not fully understood, since renal denervation interrupts renal afferent signaling to the brain and sympathetic efferent signals to the kidneys. Herein, we consider the currently proposed mechanisms involved in the development of hypertension in CIH disease models with a focus on oxidative and inflammatory mediators in the kidneys and their potential influence on renal afferent control of blood pressure, with wider consideration of the evidence available from a variety of hypertension models. We draw focus to the potential contribution of aberrant renal afferent signaling in the development, maintenance and progression of high blood pressure, which may have relevance to CIH-induced hypertension.

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Ventilatory and Autonomic Regulation in Sleep Apnea Syndrome: A Potential Protective Role for Erythropoietin?

Cited by 11 publications

References 99 publications

Potential Effects of Angiogenesis-related Factors on the Severity of APAC and Surgical Outcomes of Trabeculectomy

Potential Effects of Angiogenesis-related Factors on the Severity of APAC and Surgical Outcomes of Trabeculectomy

Erythropoietin Alleviates Burn-induced Muscle Wasting

Is Aberrant Reno-Renal Reflex Control of Blood Pressure a Contributor to Chronic Intermittent Hypoxia-Induced Hypertension?

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