Calprotectin: A protein related to cardiovascular risk in adult patients with obstructive sleep apnea

Cholidou, Kyriaki; Kostakis, Ioannis D.; Manali, Effrosyni D.; Perrea, Despina; Margeli, Alexandra; Vougas, Konstantinos; Markozannes, Evangelos; Koulouris, Nikolaos; Alchanatis, Manos

doi:10.1016/j.cyto.2012.12.014

Cited by 18 publications

(9 citation statements)

References 34 publications

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“…Plasma MRP-8/14 levels were also associated with pediatric OSAS, being suggested to reflect an increased risk for cardiovascular morbidity in children [197][198][199]. In that context, a decrease of post-CPAP treatment serum CLP levels combined with high sensitivity C-reactive protein amelioration could provide evidence for reducing post-CPAP treatment cardiovascular risk [196].…”

Section: Clp In Obstructive Sleep Apnea Syndromementioning

confidence: 99%

“…A potential role for MRP-8/14 as an inflammatory biomarker of endothelial dysfunction, a crucial characteristic of OSAS and a powerful risk-marker for cardiovascular risk, has been suggested [195]. Consequently, serum CLP may serve as a novel and reliable biomarker of cardiovascular risk severity in adult OSAS patients [196][197][198][199][200]. Plasma MRP-8/14 levels were also associated with pediatric OSAS, being suggested to reflect an increased risk for cardiovascular morbidity in children [197][198][199].…”

Section: Clp In Obstructive Sleep Apnea Syndromementioning

confidence: 99%

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Calprotectin in Lung Diseases

Kotsiou

Papagiannis

Papadopoulou

et al. 2021

IJMS

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Calprotectin (CLP) is a heterodimer formed by two S-100 calcium-binding cytosolic proteins, S100A8 and S100A9. It is a multifunctional protein expressed mainly by neutrophils and released extracellularly by activated or damaged cells mediating a broad range of physiological and pathological responses. It has been more than 20 years since the implication of S100A8/A9 in the inflammatory process was shown; however, the evaluation of its role in the pathogenesis of respiratory diseases or its usefulness as a biomarker for the appropriate diagnosis and prognosis of lung diseases have only gained attention in recent years. This review aimed to provide current knowledge regarding the potential role of CLP in the pathophysiology of lung diseases and describe how this knowledge is, up until now, translated into daily clinical practice. CLP is involved in numerous cellular processes in lung health and disease. In addition to its anti-microbial functions, CLP also serves as a molecule with pro- and anti-tumor properties related to cell survival and growth, angiogenesis, DNA damage response, and the remodeling of the extracellular matrix. The findings of this review potentially introduce CLP in daily clinical practice within the spectrum of respiratory diseases.

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Section: Clp In Obstructive Sleep Apnea Syndromementioning

confidence: 99%

Section: Clp In Obstructive Sleep Apnea Syndromementioning

confidence: 99%

Calprotectin in Lung Diseases

Kotsiou

Papagiannis

Papadopoulou

et al. 2021

IJMS

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“…; Cholidou et al . ). Although source(s) of DAMPs in CIH are unknown, they may mediate peripheral inflammation in OSA, and CIH‐induced neuroinflammation (Lehnardt et al .…”

Section: Introductionmentioning

confidence: 97%

Mechanisms of microglial activation in models of inflammation and hypoxia: Implications for chronic intermittent hypoxia

Kiernan

Smith

Mitchell

et al. 2016

The Journal of Physiology

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Chronic intermittent hypoxia (CIH) is a hallmark of sleep apnoea, a condition associated with diverse clinical disorders. CIH and sleep apnoea are characterized by increased reactive oxygen species formation, peripheral and CNS inflammation, neuronal death and neurocognitive deficits. Few studies have examined the role of microglia, the resident CNS immune cells, in models of CIH. Thus, little is known concerning their direct contributions to neuropathology or the cellular mechanisms regulating their activities during or following pathological CIH. In this review, we identify gaps in knowledge regarding CIH-induced microglial activation, and propose mechanisms based on data from related models of hypoxia and/or hypoxia-reoxygenation. CIH Abstract figure legend Putative mechanisms whereby CIH may contribute to CNS inflammation. Schematic diagram depicting three independent, but interacting, mechanisms of CIH-induced inflammation and neuropathology, and potential interactions between them. CIH increases reactive oxygen species with subsequent peripheral inflammation (1), neuronal injury (2) and microglial activation (3). Peripheral inflammation can cause CNS inflammation via diffusion of inflammatory molecules across an intact or compromised blood-brain barrier (BBB), and/or via vagal afferent neuron activation leading to secondary inflammation in the CNS, and pro-inflammatory microglial activities (A). Peripheral inflammation can induce neuronal injury or cell death by similar mechanisms (B), and/or by microglial production of pro-inflammatory or neurotoxic molecules (C). Neuron-microglial communication propagates neuroinflammation with damaged neurons or glia releasing damage-associated molecular patterns (DAMPs) into the extracellular space where they elicit microglial inflammatory activities via activation of pattern recognition receptors (e.g. Toll-like receptors) or scavenger receptors (D).

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“…Moreover, urinary cathecolamines decrease to normal levels, however without statistical significance, which could have conditioned lipid lowering effect of PAP. Treatment with PAP in OSAS may improve dyslipidemia through ameliorating hypoxia, inflammation, 73 and insulin resistance. 74 However, dyslipidemia in OSAS patients is far from being a simple process because, besides OSAS severity, several factors can contribute for it such as obesity, diet, and exercise.…”

Section: Totalmentioning

confidence: 99%

Effects of positive airway pressure therapy on cardiovascular and metabolic markers in males with obstructive sleep apnea

et al. 2017

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Introduction: Obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular/metabolic complications. Some analytical parameters (homocysteine, glycemic and lipidic profiles) are recognized markers of these consequences. Limited data is available on the association of these markers and OSAS's severity/response to positive airway pressure therapy (PAP). Material and methods: In this prospective study we analyzed polysomnographic and analytical data of male patients admitted to sleep laboratory. The aim was to evaluate metabolic/cardiovascular markers in snorers and OSAS patients, to relate with sleep parameters and PAP response. One-hundred and three patients were included, and 73 (71%) were OSAS patients. OSAS patients were similar to snorers except for higher body mass index (BMI) and dyslipidemia. Severe OSAS patients showed higher glycemia, HbA1c, insulin, and insulin resistance, and lower HDL cholesterol in comparison to mild-moderate (p < 0.05, p < 0.05, p < 0.001, p < 0.001, p < 0.05, respectively). Glycemic profile and triglycerides were slightly correlated with OSAS severity. 46 OSAS patients were submitted to 6 months of PAP,

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Calprotectin: A protein related to cardiovascular risk in adult patients with obstructive sleep apnea

Cited by 18 publications

References 34 publications

Calprotectin in Lung Diseases

Calprotectin in Lung Diseases

Mechanisms of microglial activation in models of inflammation and hypoxia: Implications for chronic intermittent hypoxia

Effects of positive airway pressure therapy on cardiovascular and metabolic markers in males with obstructive sleep apnea

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