Frontiers in physiology
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Frontiers in physiology · Jan 2020
IL-1β Induced Cytokine Expression by Spinal Astrocytes Can Play a Role in the Maintenance of Chronic Inflammatory Pain.
It is now widely accepted that the glial cells of the central nervous system (CNS) are key players in many processes, especially when they are activated via neuron-glia or glia-glia interactions. In turn, many of the glia-derived pro-inflammatory cytokines contribute to central sensitization during inflammation or nerve injury-evoked pathological pain conditions. The prototype of pro-inflammatory cytokines is interleukin-1beta (IL-1β) which has widespread functions in inflammatory processes. ⋯ We also observed that the secretion of the three cytokines is mediated by the NFkB signaling pathway. Our data completes the picture of the IL-1β-triggered cytokine cascade in spinal astrocytes, which may lead to enhanced activation of the local cells (neurons and glia as well) and can lead to the prolonged maintenance of chronic pain. All these cytokines and the NFkB pathway can be possible targets of pain therapy.
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Frontiers in physiology · Jan 2020
Value of Blood-Based microRNAs in the Diagnosis of Acute Myocardial Infarction: A Systematic Review and Meta-Analysis.
Background: Recent studies have shown that blood-based miRNAs are dysregulated in patients with acute myocardial infarction (AMI) and are therefore a potential tool for the diagnosis of AMI. Therefore, this study summarized and evaluated studies focused on microRNAs as novel biomarkers for the diagnosis of AMI from the last ten years. Methods: MEDLINE, the Cochrane Central database, and EMBASE were searched between January 2010 and December 2019. ⋯ Conclusion: miRNAs may be used as potential biomarkers for the detection of AMI. For single, stand-alone miRNAs, miRNA-499 may have better diagnostic accuracy compared to other miRNAs. We propose that a panel of multiple miRNAs with high sensitivity and specificity should be tested.
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Purpose of Review: This review summarizes the current evidence for the involvement of proteotoxicity and protein quality control systems defects in diseases of the central nervous and cardiovascular systems. Specifically, it presents the commonalities between the pathophysiology of protein misfolding diseases in the heart and the brain. Recent Findings: The involvement of protein homeostasis dysfunction has been for long time investigated and accepted as one of the leading pathophysiological causes of neurodegenerative diseases. ⋯ As a result, proteotoxicity, unfolding protein response (UPR), and ubiquitin-proteasome system (UPS) have recently been investigated as potential key pathogenic pathways and therapeutic targets for heart disease. Summary: Overall, the current knowledge summarized in this review describes how the misfolding process in the brain parallels in the heart. Understanding the folding and unfolding mechanisms involved early through studies in the heart will provide new knowledge for neurodegenerative proteinopathies and may prepare the stage for targeted and personalized interventions.
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Frontiers in physiology · Jan 2019
Submaximal Exercise Testing in Cardiovascular Rehabilitation Settings (BEST Study).
This study compared changes in measured versus predicted peak aerobic power (V̇O2peak) following cardiovascular rehabilitation (CR). Peak cardiopulmonary exercise testing (CPET) results were compared to four V̇O2peak estimation methods: the submaximal modified Bruce treadmill, Astrand-Ryhming cycle ergometer, and Chester step tests, and the Duke Activity Status Index (DASI). ⋯ Given the greater number of successful tests, no serious adverse events and acceptable mean bias, the step test appears to be a valid and safe method for assessing group-level mean changes in V̇O2peak among patients in CR. The DASI also appears to be a valid and practical questionnaire. Wide limits of agreement, however, limit their use to predict individual-level changes.
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Hepcidin, the master regulator of systemic iron homeostasis, tightly influences erythrocyte production. High hepcidin levels block intestinal iron absorption and macrophage iron recycling, causing iron restricted erythropoiesis and anemia. Low hepcidin levels favor bone marrow iron supply for hemoglobin synthesis and red blood cells production. ⋯ Compounds that antagonize hepcidin or its effect may be useful in inflammation and IRIDA, while hepcidin agonists may improve ineffective erythropoiesis. Correcting ineffective erythropoiesis in animal models ameliorates not only anemia but also iron homeostasis by reducing hepcidin inhibition. Some targeted approaches are now in clinical trials: hopefully they will result in novel treatments for a variety of anemias.