The use of combined hyperbaric oxygenation and erythropoietin in the treatment of cardiac insufficiency

Zlvković, Miodrag; Tepic, S.; Jakovljević, Vladimir; Mujovic, Vujadin M.

doi:10.2298/mpns0702025z

Cited by 4 publications

(2 citation statements)

References 2 publications

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“…The proposed binding site of R4A in C1q is in the globular region since it did not bind isolated collagen tail. This would be in agreement with the observation that the majority of anti-C1q antibodies found in lupus patients are against the globular region of C1q [30–33]. …”

Section: Discussionsupporting

confidence: 92%

Anti-DNA antibodies cross-react with C1q

Franchin

Son

Kim

et al. 2013

Journal of Autoimmunity

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Systemic lupus erythematosus (SLE) is an autoimmune disorder that involves multiple organ systems and typically presents as a chronic inflammatory disease. Antibodies to double-stranded (ds) DNA are present in approximately 70% of patients and form nucleic acid containing immune complexes which activate dendritic cells through engagement of toll-like receptors, leading to a pro-inflammatory, pro-immunogenic milieu. In addition, anti-dsDNA antibodies deposit in kidneys to initiate glomerulonephritis. Antibodies to C1q have also been implicated in lupus nephritis and are found in 30–50% of patients. C1q is a known suppressor of immune activation and C1q deficiency is the strongest risk factor for SLE. We previously identified a subset of anti-DNA antibodies that binds the N-methyl-d-aspartate receptor. We now show that both mouse and human anti-DNA antibodies with this specificity bind C1q. These antibodies bind to Clq in glomeruli and exhibit decreased glomerular deposition in the absence of C1q. We propose that this subset of anti-DNA antibodies participates in lupus pathogenesis through direct targeting of C1q on glomeruli and also through removal of soluble C1q thereby limiting the ability of C1q to mediate immune homeostasis.

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Section: Discussionsupporting

confidence: 92%

Anti-DNA antibodies cross-react with C1q

Franchin

Son

Kim

et al. 2013

Journal of Autoimmunity

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“…Interestingly, the combination of HBO with erythropoietin in experimental rat spinal cord injury ( 90 ) and in humans diagnosed with cardiac insufficiency ( 91 ) offered promising results on combining HBO treatment with other agents.…”

Section: The Effects Of Hbo Treatment In Experimental Hypoxia-ischemiamentioning

confidence: 99%

Hyperbaric oxygen therapy for the treatment of hypoxic/ischemic injury upon perinatal asphyxia—are we there yet?

Mielecki,

Godlewski,

Salinska

2024

Front. Neurol.

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Birth asphyxia and its main sequel, hypoxic-ischemic encephalopathy, are one of the leading causes of children’s deaths worldwide and can potentially worsen the quality of life in subsequent years. Despite extensive research efforts, efficient therapy against the consequences of hypoxia-ischemia occurring in the perinatal period of life is still lacking. The use of hyperbaric oxygen, improving such vital consequences of birth asphyxia as lowered partial oxygen pressure in tissue, apoptosis of neuronal cells, and impaired angiogenesis, is a promising approach. This review focused on the selected aspects of mainly experimental hyperbaric oxygen therapy. The therapeutic window for the treatment of perinatal asphyxia is very narrow, but administering hyperbaric oxygen within those days improves outcomes. Several miRNAs (e.g., mir-107) mediate the therapeutic effect of hyperbaric oxygen by modulating the Wnt pathway, inhibiting apoptosis, increasing angiogenesis, or inducing neural stem cells. Combining hyperbaric oxygen therapy with drugs, such as memantine or ephedrine, produced promising results. A separate aspect is the use of preconditioning with hyperbaric oxygen. Overall, preliminary clinical trials with hyperbaric oxygen therapy used in perinatal asphyxia give auspicious results.

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Autoantibodies against complement components in systemic lupus erythematosus – role in the pathogenesis and clinical manifestations

Hristova¹,

Stoyanova

2017

Lupus

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Many complement structures and a number of additional factors, i.e. autoantibodies, receptors, hormones and cytokines, are implicated in the complex pathogenesis of systemic lupus erythematosus. Genetic defects in the complement as well as functional deficiency due to antibodies against its components lead to different pathological conditions, usually clinically presented. Among them hypocomplementemic urticarial vasculitis, different types of glomerulonephritis as dense deposit disease, IgA nephropathy, atypical haemolytic uremic syndrome and lupus nephritis are very common. These antibodies cause conformational changes leading to pathological activation or inhibition of complement with organ damage and/or limited capacity of the immune system to clear immune complexes and apoptotic debris. Finally, we summarize the role of complement antibodies in the pathogenesis of systemic lupus erythematosus and discuss the mechanism of some related clinical conditions such as infections, thyroiditis, thrombosis, acquired von Willebrand disease, etc.

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The use of combined hyperbaric oxygenation and erythropoietin in the treatment of cardiac insufficiency

Cited by 4 publications

References 2 publications

Anti-DNA antibodies cross-react with C1q

Anti-DNA antibodies cross-react with C1q

Hyperbaric oxygen therapy for the treatment of hypoxic/ischemic injury upon perinatal asphyxia—are we there yet?

Autoantibodies against complement components in systemic lupus erythematosus – role in the pathogenesis and clinical manifestations

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