scholarly journals Visfatin Connection: Present and Future in Osteoarthritis and Osteoporosis

2019 ◽  
Vol 8 (8) ◽  
pp. 1178 ◽  
Author(s):  
Eloi Franco-Trepat ◽  
María Guillán-Fresco ◽  
Ana Alonso-Pérez ◽  
Alberto Jorge-Mora ◽  
Vera Francisco ◽  
...  

Musculoskeletal pathologies (MSPs) such as osteoarthritis (OA) and osteoporosis (OP), are a set of disorders that cause severe pain, motion difficulties, and even permanent disability. In developed countries, the current incidence of MSPs reaches about one in four adults and keeps escalating as a consequence of aging and sedentarism. Interestingly, OA and OP have been closely related to similar risk factors, including aging, metabolic alterations, and inflammation. Visfatin, an adipokine with an inflammatory and catabolic profile, has been associated with several OA and OP metabolic risk factors, such as obesity, insulin resistance, and type II diabetes. Furthermore, visfatin has been associated with the innate immune receptor toll-like receptor 4 (TLR4), which plays a key role in cartilage and bone inflammatory and catabolic responses. Moreover, visfatin has been related to several OA and OP pathologic features. The aim of this work is to bring together basic and clinical data regarding the common role of visfatin in these pathologies and their major shared risk factors. Finally, we discuss the pitfalls of visfatin as a potential biomarker and therapeutic target in both pathologies.

VASA ◽  
2017 ◽  
Vol 46 (5) ◽  
pp. 347-353 ◽  
Author(s):  
Frederic Baumann ◽  
Deborah Hehli ◽  
Vladimir Makaloski ◽  
Martin Schumacher ◽  
Heinz Schönhofen ◽  
...  

Abstract. Erectile dysfunction (ED) is an evolving health problem with growing incidence in the ageing male population with potentially predictive value for cardiovascular and other chronic diseases. ED shares the common cardiovascular risk factors. The aetiology of ED is numerous including neurogenic, psychogenic, arteriogenic, and venogenic reasons. The origin of arteriogenic ED is frequently atherosclerosis. Patients not adequately responding to conservative measures including oral medication are often referred to further vascular diagnostics and therapy. At present, the refinements in endovascular therapy allow for minimal-invasive revascularization of erection-related arteries. The role of endovascular therapy in the complex framework of the multifactorial causes of ED requires further scientific scrutiny.


Hematology ◽  
2005 ◽  
Vol 2005 (1) ◽  
pp. 442-444 ◽  
Author(s):  
David Ginsburg

Abstract Arterial thrombosis is a central pathologic mechanism contributing to myocardial infarction and stroke, together the leading causes of death in developed countries. This article reviews the current state of knowledge concerning the role of inherited variation in hemostatic and inflammatory factor genes in determining the risk of arterial thrombosis/ischemic heart disease. Despite considerable progress in identifying important genetic risk factors underlying predisposition to venous thrombosis, the genetic factors contributing to the risk for arterial thrombosis remain largely unknown. However, the rapid development of powerful new genomic resources should facilitate considerably more sophisticated analyses, leading to novel insight into the molecular pathophysiology of this important set of human diseases.


2018 ◽  
Vol 24 (3) ◽  
pp. 281-290 ◽  
Author(s):  
Peter Riis Hansen

Inflammation plays a significant role in atherosclerosis and cardiovascular disease (CVD). Patients with chronic inflammatory diseases are at increased risk of CVD, but it is debated whether this association is causal or dependent on shared risk factors, other exposures, genes, and/or inflammatory pathways. The current review summarizes epidemiological, clinical, and experimental data supporting the role of shared inflammatory mechanisms between atherosclerotic CVD and rheumatoid arthritis, psoriasis, inflammatory bowel disease, and periodontitis, respectively, and provides insights to future prospects in this area of research. Awareness of the role of inflammation in CVD in patients with chronic inflammatory diseases and the potential for anti-inflammatory therapy, e.g., with tumor necrosis factor-α inhibitors, to also reduce atherosclerotic CVD has evolved into guideline- based recommendations. These include regular CVD risk assessment, aggressive treatment of traditional CVD risk factors, and recognition of reduced CVD as an added benefit of strict inflammatory disease control. At present, chronic inflammatory diseases would appear to qualify as partners in crime and not merely innocent bystanders to CVD. However, definite incremental contributions of inflammation versus effects of the complex interplay with other CVD risk factors may never be fully elucidated and for the foreseeable future, inflammation is posed to maintain its current position as both a marker and a maker of CVD, with clinical utility both for identification of patient at risk of CVD and as target for therapy to reduce CVD.


2012 ◽  
Vol 23 (7) ◽  
pp. 991-1008 ◽  
Author(s):  
Adedayo A. Onitilo ◽  
Jessica M. Engel ◽  
Ingrid Glurich ◽  
Rachel V. Stankowski ◽  
Gail M. Williams ◽  
...  
Keyword(s):  

2017 ◽  
Vol 69 (4) ◽  
pp. 498-505 ◽  
Author(s):  
Andrea G. Kattah ◽  
Dawn C. Scantlebury ◽  
Sanket Agarwal ◽  
Michelle M. Mielke ◽  
Walter A. Rocca ◽  
...  
Keyword(s):  

Genes ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 13
Author(s):  
Mengchen Zhou ◽  
Jiangtao Dong ◽  
Lingfeng Zha ◽  
Yuhua Liao

Observational studies have revealed that dental diseases such as periodontitis and dental caries increase the risk of cardiovascular diseases (CVDs). However, the causality between periodontal disease (PD) and CVDs is still not clarified. In the present study, two-sample Mendelian randomization (MR) studies were carried out to assess the association between genetic liability for periodontal diseases (dental caries and periodontitis) and major CVDs, including coronary artery disease (CAD), heart failure (HF), atrial fibrillation (AF), and stroke—including ischemic stroke as well as its three main subtypes—based on large-scale genome-wide association studies (GWASs). Our two-sample MR analyses did not provide evidence for dental caries and periodontitis as the causes of cardiovascular diseases; sensitivity analyses, including MR–Egger analysis and weighted median analysis, also supported this result. Gene functional annotation and pathway enrichment analyses indicated the common pathophysiology between cardiovascular diseases and periodontal diseases. The associations from observational studies may be explained by shared risk factors and comorbidities instead of direct consequences. This also suggests that addressing the common risk factors—such as reducing obesity and improving glucose tolerance—could benefit both conditions.


2010 ◽  
Vol 24 (1) ◽  
pp. 1-20 ◽  
Author(s):  
Siobhan Muldowney ◽  
Mairead Kiely

The cardiometabolic syndrome (MetS) is a clustering of related metabolic abnormalities including abdominal adiposity, insulin resistance, hypertension, dyslipidaemia and increased inflammatory and thrombotic markers, which is linked to increased risk of type 2 diabetes, CVD and overall mortality. Several cross-sectional and prospective studies have shown an association between low vitamin D status, as indicated by concentrations of serum 25-hydroxyvitamin D (s25(OH)D), and increased prevalence of the MetS and individual CVD risk factors. These epidemiological observations are supported by mechanistic studies but experimental data are limited. The available data from intervention studies are largely confounded as most vitamin D supplementation trials were mainly carried out to explore the role of Ca in CVD and include Ca in the treatment arms. Inadequate consideration of seasonal effects on s25(OH)D concentrations is also a common design flaw in most studies. Further complications arise from shared risk factors such as adiposity and ageing, which predispose individuals to exhibit both a more pronounced risk profile and relatively lower s25(OH)D concentrations. In conclusion, while epidemiological associations are promising and a rationale for low vitamin D status as a potentially modifiable risk factor for CVD is supported by mechanistic data, suitable experimental data from appropriately designed trials are just beginning to emerge. As yet, this body of literature is too immature to draw firm conclusions on the role of vitamin D in CVD prevention. Carefully controlled vitamin D trials in well-described population groups using intervention doses that are titrated against target s25(OH)D concentrations could yield potentially valuable outcomes that may have a positive impact on CVD risk modification.


2021 ◽  
pp. S153-S159
Author(s):  
L MÁČOVÁ ◽  
M BIČÍKOVÁ ◽  
R HAMPL

Aged people are the most susceptible group to COVID-19 infection. Immunosenescence characterized by impairment of immune function with inflamm-aging contributes to pathophysiological alterations, among which endocrine and metabolic diseases are not exception. Diabetes, obesity along with impairment of disorders of thyroid functions are the most frequent ones, the common feature of which is failure of immune system including autoimmune processes. In the minireview we discussed how COVID-19 and aging impact innate and adaptive immunity, diabetes and selected neuroendocrine processes. Mentioned is also beneficial effect of vitamin D for attenuation of these diseases and related epigenetic issues. Particular attention is devoted to the role of ACE2 protein in the light of its intimate link with renin-angiotensin regulating system.


2021 ◽  
pp. svn-2021-001157
Author(s):  
Mengmeng Shi ◽  
Xinyi Leng ◽  
Ying Li ◽  
Zihan Chen ◽  
Ye Cao ◽  
...  

ObjectivesThe predisposition of intracranial atherosclerotic disease (ICAD) to East Asians over Caucasians infers a genetic basis which, however, remains largely unknown. Higher prevalence of vascular risk factors (VRFs) in Chinese over Caucasian patients who had a stroke, and shared risk factors of ICAD with other stroke subtypes indicate genes related to VRFs and/or other stroke subtypes may also contribute to ICAD.MethodsUnrelated symptomatic patients with ICAD were recruited for genome sequencing (GS, 60-fold). Rare and potentially deleterious single-nucleotide variants (SNVs) and small insertions/deletions (InDels) were detected in genome-wide and correlated to genes related to VRFs and/or other stroke subtypes. Rare aneuploidies, copy number variants (CNVs) and chromosomal structural rearrangements were also investigated. Lastly, candidate genes were used for pathway and gene ontology enrichment analysis.ResultsAmong 92 patients (mean age at stroke onset 61.0±9.3 years), GS identified likely ICAD-associated rare genomic variants in 54.3% (50/92) of patients. Forty-eight patients (52.2%, 48/92) had 59 rare SNVs/InDels reported or predicted to be deleterious in genes related to VRFs and/or other stroke subtypes. None of the 59 rare variants were identified in local subjects without ICAD (n=126). 31 SNVs/InDels were related to conventional VRFs, and 28 were discovered in genes related to other stroke subtypes. Our study also showed that rare CNVs (n=7) and structural rearrangement (a balanced translocation) were potentially related to ICAD in 8.7% (8/92) of patients. Lastly, candidate genes were significantly enriched in pathways related to lipoprotein metabolism and cellular lipid catabolic process.ConclusionsOur GS study suggests a role of rare genomic variants with various variant types contributing to the development of ICAD in Chinese patients.


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