CALCIUM AND VITAMIN : EFFECTS ON BONE TISSUE AND VASCULAR REMODELING (LITERATURE REVIEW)

2021 ◽  
pp. 1200-1208
Author(s):  
С. В. Булгакова ◽  
Е. В. Тренева ◽  
Н. О. Захарова ◽  
А. В. Николаева

Препараты кальция входят в схемы лечения и профилактики низкой минеральной плотности костной ткани. Однако последние научные исследования показали, что дополнительное поступление кальция может увеличить риск сердечно-сосудистых заболеваний. Это связано с отложением кальция в эндотелии кровеносных сосудов. Значимость минерализации сосудистой стенки не ограничивается локальным накоплением кальциевых депозитов, но в значительной мере определяется их активирующим влиянием на прогрессирование атеросклероза. Витамин К играет важную роль в гомеостазе кальция, снижает артериальную кальцификацию и артериальную жесткость и, как следствие, оказывает протективный эффект при приеме кальция. В данном обзоре литературы представлена современная информация о кальциевом парадоксе, обсуждаются основные молекулярные механизмы кальцификации сосудов, рассмотрены терапевтические стратегии лечения витамином К . Calcium preparations are included in the treatment and prevention regimens for low bone mineral density. However, recent scientific studies have shown that additional calcium intake can increase the risk of heart disease, which is associated with the deposition of calcium in the endothelium of blood vessels. The significance of vascular wall mineralization is not limited to local accumulation of calcium deposits, but is largely determined by their activating effect on the progression of atherosclerosis. Vitamin K plays an important role in calcium homeostasis, reduces arterial calcification and arterial stiffness and, as a result, has a protective effect when taking calcium. This literature review provides current information about the calcium paradox, discusses the main molecular mechanisms of vascular calcification, and considers therapeutic strategies for vitamin К treatment.

2001 ◽  
Vol 280 (3) ◽  
pp. F365-F388 ◽  
Author(s):  
Raghvendra K. Dubey ◽  
Edwin K. Jackson

A number of cellular and biochemical processes are involved in the pathophysiology of glomerular and vascular remodeling, leading to renal and vascular disorders, respectively. Although estradiol protects the renal and cardiovascular systems, the mechanisms involved remain unclear. In this review we provide a discussion of the cellular, biochemical, and molecular mechanisms by which estradiol may exert protective effects on the kidneys and vascular wall. In this regard, we consider the possible role of genomic vs. nongenomic mechanisms and estrogen receptor-dependent vs. estrogen receptor-independent mechanisms in mediating the protective effects of estradiol on the renal and cardiovascular systems.


Author(s):  
◽  
Eptisam lambu

Pulmonary arterial hypertension (PAH) is a rare multifactorial disease characterized by abnormal high blood pressure in the pulmonary artery, or increased pulmonary vascular resistance (PVR), caused by obstruction in the small arteries of the lung. Increased PVR is also thought to be caused by abnormal vascular remodeling, due to thickening of the pulmonary vascular wall resulting from significant hypertrophy of pulmonary arterial smooth-muscle cells (PASMCs) and increased proliferation/impaired apoptosis of pulmonary arterial endothelial cells (PAECs). Herein, we investigated the mechanisms and explored molecular pathways mediating the lung pathogenesis in two PAH rat models: Monocrotaline (MCT) and Sugen5416/Hypoxia (SuHx). We analyzed these disease models to determine where the vasculature shows the most severe PAH pathology and which model best recapitulates the human disease. We investigated the role vascular remodeling, hypoxia, cell proliferation, apoptosis, DNA damage and inflammation play in the pathogenesis of PAH. Neither model recapitulated all features of the human disease, however each model presented with some of the pathology seen in PAH patients.


2020 ◽  
pp. 39-43
Author(s):  
A. V. Voronkina ◽  
T. A. Raskina ◽  
M. V. Letaeva ◽  
Yu. V. Averkieva ◽  
O. S. Malyshenko ◽  
...  

The development of atherosclerosis is closely related to the calcification of the vessel intima and fibrous plaques, being a complex and multifactorial process, in which the markers of bone formation and resorption play an important role. Objective. To study the biochemical markers of bone metabolism in men with stable coronary heart disease (CHD). Material and methods. The study included 102 men with verified CHD. Data were evaluated by densitometry, coronary angiography, multispiral computed tomography, color duplex scanning of brachiocephalic arteries, serum lipids (total cholesterol, triglycerides [TG], high-density [LHD] and low-density lipoprotein cholesterol), concentrationsin the blood of osteocalcin (OC), bone alkaline phosphatase (BAP), cathepsin K and C-telopeptides (CTx). Results. Concentrations of BAP, cathepsin K and CTx in patients with CHD were significantly higher than in men without CHD. The concentration of OC in men with normal bone mineral density was significantly lower than in patients with osteopenic syndrome. There was a direct correlation between OC and antiatherogenic HDL cholesterol and the inverse correlation between OC and TG, CTx and TG. There was no correlation between the level of bone remodeling markers and coronary artery (CA) lesion variant and the severity of coronary atherosclerosis on SYNTAX scale. The correlation analysis did not reveal the connection of biochemical markers of bone metabolism with the severity of coronary atherosclerosis and calcification and thickness of intima-media complex of carotid arteries. Absolute values of bone formation indices (BAP, OC) were significantly higher in patients with severe СA calcification than in patients without signs of calcification. Summary. Increased rates of osteogenesis and osteoresorption characterize the accelerated process of bone metabolism and indicate in favor of high rates of bone loss in men with CHD, which confirms the likelihood of common pathophysiological mechanisms of bone resorption and arterial calcification.


2020 ◽  
Vol 20 (13) ◽  
pp. 1014-1022 ◽  
Author(s):  
Suresh Mallepalli ◽  
Manoj Kumar Gupta ◽  
Ramakrishna Vadde

Background: Neuroblastoma (NB) is the second leading extracranial solid tumors of early childhood and clinically characterized by the presence of round, small, monomorphic cells with excess nuclear pigmentation (hyperchromasia).Owing to a lack of definitive treatment against NB and less survival rate in high-risk patients, there is an urgent requirement to understand molecular mechanisms associated with NB in a better way, which in turn can be utilized for developing drugs towards the treatment of NB in human. Objectives: In this review, an approach was adopted to understand major risk factors, pathophysiology, the molecular mechanism associated with NB, and various therapeutic agents that can serve as drugs towards the treatment of NB in humans. Conclusions: Numerous genetic (e.g., MYCN amplification), perinatal, and gestational factors are responsible for developing NB. However, no definite environmental or parental exposures responsible for causing NB have been confirmed to date. Though intensive multimodal treatment approaches, namely, chemotherapy, surgery &radiation, may help in improving the survival rate in children, these approaches have several side effects and do not work efficiently in high-risk patients. However, recent studies suggested that numerous phytochemicals, namely, vincristine, and matrine have a minimal side effect in the human body and may serve as a therapeutic drug during the treatment of NB. Most of these phytochemicals work in a dose-dependent manner and hence must be prescribed very cautiously. The information discussed in the present review will be useful in the drug discovery process as well as treatment and prevention on NB in humans.


2019 ◽  
Vol 19 (3) ◽  
pp. 259-273 ◽  
Author(s):  
Neelam Kaushal ◽  
Divya Vohora ◽  
Rajinder K Jalali ◽  
Sujeet Jha

Background And Objective:Osteoporosis is a common bone disorder that increases susceptibility to fragility bone fractures. The clinical and public health repercussions of osteoporosis are huge due to the morbidity, mortality, and cost of medical care linked with fragility fractures. Clinical assessment of osteoporotic risk factors can help to identify candidates at an early stage that will benefit from medical intervention and potentially lowering the morbidity and mortality seen with fractures and complications. Given this, research is ongoing to evaluate the association of osteoporosis with some novel or less well-studied risk factors/bio-markers such as uric acid (UA).Discussion:Uric acid’s antioxidant activity has been proposed to be one of the factors responsible for increasing longevity and lowering rates of age-related cancers during primate evolution, the level of which increased markedly due to loss of uricase enzyme activity (mutational silencing). Accumulated evidence shows that oxidative stress is the fundamental mechanism of age-related bone loss and acts via enhancing osteoclastic activity and increasing bone resorption. Antioxidant substances such as ascorbic acid scavenge free radicals are positively related to bone health. Thus, it is hypothesized that uric acid holds bone-protective potential owing to its potent antioxidative property. Several correlation studies have been conducted globally to investigate the relationship between serum uric acid with bone mineral density and osteoporosis. Few pre-clinical studies have tried to investigate the interaction between uric acid and bone mineral density and reported important role played via Runt-related transcription factor 2 (RUNX2)/core-binding factor subunit alpha-1 (CBF-alpha-1), Wingless-related integration site (Wnt)-3a/β-catenin signaling pathway and 11β Hydroxysteroid Dehydrogenase type 1.Conclusion:In this review, the authors provided a comprehensive summary of the literature related to association studies reported in humans as well work done until date to understand the potential cellular and molecular mechanisms that interplay between uric acid and bone metabolism.


2011 ◽  
Vol 33 (3) ◽  
pp. 250-259 ◽  
Author(s):  
Joseph Gawdzik ◽  
Liby Mathew ◽  
Gene Kim ◽  
Tipu S. Puri ◽  
Marion A. Hofmann Bowman

Antibiotics ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 437
Author(s):  
Ilaria Maria Saracino ◽  
Matteo Pavoni ◽  
Angelo Zullo ◽  
Giulia Fiorini ◽  
Tiziana Lazzarotto ◽  
...  

Background and aims: Only a few antimicrobials are effective against H. pylori, and antibiotic resistance is an increasing problem for eradication therapies. In 2017, the World Health Organization categorized clarithromycin resistant H. pylori as a “high-priority” bacterium. Standard antimicrobial susceptibility testing can be used to prescribe appropriate therapies but is currently recommended only after the second therapeutic failure. H. pylori is, in fact, a “fastidious” microorganism; culture methods are time-consuming and technically challenging. The advent of molecular biology techniques has enabled the identification of molecular mechanisms underlying the observed phenotypic resistance to antibiotics in H. pylori. The aim of this literature review is to summarize the results of original articles published in the last ten years, regarding the use of Next Generation Sequencing, in particular of the whole genome, to predict the antibiotic resistance in H. pylori.Methods: a literature research was made on PubMed. The research was focused on II and III generation sequencing of the whole H. pylori genome. Results: Next Generation Sequencing enabled the detection of novel, rare and complex resistance mechanisms. The prediction of resistance to clarithromycin, levofloxacin and amoxicillin is accurate; for other antimicrobials, such as metronidazole, rifabutin and tetracycline, potential genetic determinants of the resistant status need further investigation.


2021 ◽  
Vol 22 (6) ◽  
pp. 3238
Author(s):  
Ho-Wei Hsu ◽  
Ting-Yi Lin ◽  
Yi-Ching Liu ◽  
Jwu-Lai Yeh ◽  
Jong-Hau Hsu

The ductus arteriosus (DA) is a physiologic vessel crucial for fetal circulation. As a major regulating factor, the prostaglandin pathway has long been the target for DA patency maintenance or closure. However, the adverse effect of prostaglandins and their inhibitors has been a major unsolved clinical problem. Furthermore, a significant portion of patients with patent DA fail to respond to cyclooxygenase inhibitors that target the prostaglandin pathway. These unresponsive medical patients ultimately require surgical intervention and highlight the importance of exploring pathways independent from this well-recognized prostaglandin pathway. The clinical limitations of prostaglandin-targeting therapeutics prompted us to investigate molecules beyond the prostaglandin pathway. Thus, this article introduces molecules independent from the prostaglandin pathway based on their correlating mechanisms contributing to vascular remodeling. These molecules may serve as potential targets for future DA patency clinical management.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 838.2-838
Author(s):  
L. Marchenkova ◽  
V. Vasileva

Background:There is a high prevalence of osteoporosis (OP) among patients of the older age undergoing rehabilitation. Therefore, it is obvious that physicians working in the field of physical and rehabilitative medicine should be well oriented in this medical problem.Objectives:to study the relevance of the problem of osteoporosis (OP) for physicians working in the field of physical and rehabilitation medicine, their awareness of the main methods of diagnosis, treatment and prevention of this disease, as well as the frequency of their use in daily clinical activities.Methods:A cross-type study was carried out using a questionnaire survey. The study included 157 doctors (M-34, F-123) of 8 medical specialties working in 27 specialized medical institutions on the profile of “medical rehabilitation. The questionnaire for doctors consisted of 21 items of special questions.Results:90.45% of the surveyed doctors believed that the problem of OP is relevant for their clinical activities, 100% of the respondents indicated that the presence of OP significantly affects the rehabilitation prognosis and 95.54% - on the degree of effectiveness of medical rehabilitation. According to the respondents, patients with OP make up on average 30.0% [20.0; 50.0] (0-90) of the total flow of patients. 92.36% (145/157) of doctors indicated that they know the risk factors for OP, 98.73% (155/157) - methods for diagnosing OP, 68.79% (108/157) - methods for treating OP, 80.25 % (126/157) - methods of preventing OP, 47.13% (74/157) - what is FRAX. However, 35.01% (55/157) of the respondents considered their level of awareness of the problem sufficient for managing patients with OP. Diagnostic procedures for OP are recommended by all endocrinologists (100%) and the majority of traumatologists (72.73%), gynecologists (66.67) and cardiologists (64.28%), as well as on average half (50%) neurologists and therapists. Endocrinologists (100%), gynecologists (66.67%) and therapists (60%) are mainly involved in the treatment of OP. 32.48% (51/157) of physicians have ever referred their patients to a bone mineral density assessment.Conclusion:Conclusion. The problem of OP is relevant for the clinical activities of specialists in physical and rehabilitation medicine, and there is the need for advanced training on the problem of OP among these specialists.Disclosure of Interests:None declared.


2013 ◽  
Vol 93 (4) ◽  
pp. 1743-1802 ◽  
Author(s):  
Jean-Sébastien Silvestre ◽  
David M. Smadja ◽  
Bernard I. Lévy

After the onset of ischemia, cardiac or skeletal muscle undergoes a continuum of molecular, cellular, and extracellular responses that determine the function and the remodeling of the ischemic tissue. Hypoxia-related pathways, immunoinflammatory balance, circulating or local vascular progenitor cells, as well as changes in hemodynamical forces within vascular wall trigger all the processes regulating vascular homeostasis, including vasculogenesis, angiogenesis, arteriogenesis, and collateral growth, which act in concert to establish a functional vascular network in ischemic zones. In patients with ischemic diseases, most of the cellular (mainly those involving bone marrow-derived cells and local stem/progenitor cells) and molecular mechanisms involved in the activation of vessel growth and vascular remodeling are markedly impaired by the deleterious microenvironment characterized by fibrosis, inflammation, hypoperfusion, and inhibition of endogenous angiogenic and regenerative programs. Furthermore, cardiovascular risk factors, including diabetes, hypercholesterolemia, hypertension, diabetes, and aging, constitute a deleterious macroenvironment that participates to the abrogation of postischemic revascularization and tissue regeneration observed in these patient populations. Thus stimulation of vessel growth and/or remodeling has emerged as a new therapeutic option in patients with ischemic diseases. Many strategies of therapeutic revascularization, based on the administration of growth factors or stem/progenitor cells from diverse sources, have been proposed and are currently tested in patients with peripheral arterial disease or cardiac diseases. This review provides an overview from our current knowledge regarding molecular and cellular mechanisms involved in postischemic revascularization, as well as advances in the clinical application of such strategies of therapeutic revascularization.


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