Laura Martínez-Arias's research while affiliated with University of Oviedo and other places
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Publications (17)
Vascular calcification (VC) is a common complication in patients with chronic kidney disease which increases their mortality. Although oxidative stress is involved in the onset and progression of this disorder, the specific role of some of the main redox regulators, such as catalase, the main scavenger of H2O2, remains unclear. In the present study...
Vascular calcification (VC), is a common complication in patients with chronic kidney disease and increases mortality. Although oxidative stress is involved in the onset and progression of this disorder, the specific role of some main redox regulators such as catalase, the main scavenger of H2O2, remains unclear. In the present study, epigastric ar...
Preclinical biomedical models are a fundamental tool to improve the knowledge and management of diseases, particularly in diabetes mellitus (DM) since, currently, the pathophysiological and molecular mechanisms involved in its development are not fully clarified, and there is no treatment to cure DM. This review will focus on the features, advantag...
Drugs providing antihypertensive and protective cardiovascular actions are of clinical interest in controlling cardiovascular events and slowing the progression of kidney disease. We studied the effect of a hybrid compound, GGN1231 (derived from losartan in which a powerful antioxidant was attached), on the prevention of cardiovascular damage, card...
In chronic kidney disease, systemic inflammation and high serum phosphate (P) promote the de-differentiation of vascular smooth muscle cells (VSMC) to osteoblast-like cells, increasing the propensity for medial calcification and cardiovascular mortality. Vascular microRNA-145 (miR-145) content is essential to maintain VSMC contractile phenotype. Be...
Background and objective:
Adequate serum phosphorus levels in patients with chronic kidney disease is essential for their clinical management. However, the control of hyperphosphatemia is difficult because is normally associated with increases in serum PTH. In the present study, the effects of hyperphosphatemia, in the presence of elevated and nor...
In the course of chronic kidney disease (CKD), alterations in the bone-vascular axis augment the risk of bone loss, fractures, vascular and soft tissue calcification, left ventricular hypertrophy, renal and myocardial fibrosis, which markedly increase morbidity and mortality rates. A major challenge to improve skeletal and cardiovascular outcomes i...
Background and objective:
Adequate serum phosphorus levels in patients with chronic kidney disease is essential for their clinical management. However, the control of hyperphosphatemia is difficult because is normally associated with increases in serum PTH. In the present study, the effects of hyperphosphatemia, in the presence of elevated and nor...
Background
In chronic kidney Disease (CKD) the activation of the renin-angiotensin-aldosterone system and renal inflammation stimulate renal fibrosis and the progression to end-stage renal disease. The low levels of vitamin D receptor (VDR) and its activators (VDRAs) contribute to worsen secondary hyperparathyroidism and renal fibrosis.
Methods
Th...
Fibrosis is a process characterized by an excessive accumulation of the extracellular matrix as a response to different types of tissue injuries, which leads to organ dysfunction. The process can be initiated by multiple and different stimuli and pathogenic factors which trigger the cascade of reparation converging in molecular signals responsible...
Background:
In chronic kidney disease, serum phosphorus (P) elevations stimulate parathyroid hormone (PTH) production, causing severe alterations in the bone-vasculature axis. PTH is the main regulator of the receptor activator of nuclear factor κB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system, which is essential for bone maintenance and...
In chronic kidney disease (CKD), hyperphosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal and vascular injury, and TNFα-induction of neutral-sphingomyelinase2 (nSMase2) to release pro-calcifying exosomes. This study examined anti-i...
In mammalians, advancing age is associated with sarcopenia, the progressive and involuntary loss of muscle mass and strength. Hyperphosphatemia is an aging-related condition involved in several pathologies. The aim of this work was to assess whether hyperphosphatemia plays a role in the age-related loss of mass muscle and strength by inducing cellu...
Background
Bicuspid aortic valve (BAV) is a heterogeneous and still not fully understood condition, with diverse genetic etiology and associated phenotypes ranging from aortic stenosis or regurgitation to aneurysm and dissection. Several genes have been associated with the presence of BAV, notably some members of the GATA family of transcription fa...
Background:
In chronic kidney disease (CKD), increases in serum phosphate and parathyroid hormone (PTH) aggravate vascular calcification (VC) and bone loss. This study was designed to discriminate high phosphorus (HP) and PTH contribution to VC and bone loss.
Methods:
Nephrectomized rats fed a HP diet underwent either sham operation or parathyro...
Background.:
Uraemic cardiomyopathy, a process mainly associated with increased myocardial fibrosis, is the leading cause of death in chronic kidney disease patients and can be prevented by vitamin D receptor activators (VDRAs). Since some microRNAs (miRNAs) have emerged as regulators of the fibrotic process, we aimed to analyse the role of specif...
Vascular calcification is a frequent cause of morbidity and mortality in patients with CKD and the general population. The common association between vascular calcification and osteoporosis suggests a link between bone and vascular disorders. Because microRNAs (miRs) are involved in the transdifferentiation of vascular smooth muscle cells into oste...
Citations
... Among these multifarious effects, the findings of several studies have indicated that miRNAs are involved in the osteogenic differentiation of VSMCs. For example, it has been established that by promoting the expression of miR-145, vitamin D attenuates the uremia-induced osteogenic differentiation of the aorta [24], whereas miRNA-223-3p has been demonstrated to inhibit the osteogenic switch of VSMCs [25]. Notably, whereas a few miRNAs have been found to play an inhibitory role in osteogenic differentiation, others promote this process [26]. ...
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... This process leads to apoptosis or necrosis of cardiomyocytes which are replaced by fibroblasts and extracellular collagen with the consequent progression of fibrosis [7,8]. Experimental induction of moderate and severe chronic renal failure (CRF) leads not only to the development of cardiac hypertrophy and fibrosis [9,10] but also to vascular damage that, in the last instance, might be conducive to the appearance of vascular calcification [11]. ...
... They contribute to fibrosis through different mechanisms, including direct activation of TGF-β and the noncanonical pathways as well as upregulation of other pathways such as the RAAS system. CKD-MBD features that have been related to fibrosis include hyperparathyroidism [13,105], upregulation of FGF-23 [106,107], Klotho decrease [108] and vitamin D deficiency [109][110][111]. ...
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... Regarding kidney injury, the activation of Wnt signaling appears to have reparative effects in AKI, but its sustained activation becomes deleterious in CKD [32,33]. DKK1, an inhibitor of the LRP5/6 co-receptor, has been used in several studies to interrupt classical Wnt signaling [34]. Notably, DKK1 can inhibit myofibroblast activation and, ultimately, fibrosis in mice with obstructive injury [35]. ...
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... The role of VDR extends into the broader spectrum of chronic kidney disease, where its diminished levels and activity exacerbate conditions like secondary hyperparathyroidism and renal fibrosis (Bakdash et al., 2014;Barragan et al., 2015). This insight gains practical significance in experimental models of chronic renal failure (CRF), where VDR agonists like paricalcitol and calcitriol have demonstrated remarkable anti-fibrotic effects, offering a therapeutic window (Martínez-Arias et al., 2021). Moreover, the genetic landscape of VDR in kidney diseases has been illuminated by a comprehensive meta-analysis. ...
... Given the role of LGR4 in osteoblast differentiation, it is reasonable to speculate that it could be involved in the differentiation of VSMCs into osteoblast-like cells, thereby affecting vascular calcification. In the vasculature, the increase in RANKL and the decrease in OPG are known to promote vascular calcification [10,11], and recent evidence suggests that these changes are accompanied by an upregulation of LGR4 expression [12]. In fact, LGR4 has been detected in the calcified areas of the arteries from uremic rats. ...
... Over time, the renal function of all individuals with chronic renal disease gradually deteriorates. The process is typically irreversible, resulting in end-stage renal failure, necessitating kidney transplantation or lifelong dialysis (Panizo et al. 2021). The last pathway that connects all kidney disorders to chronic renal failure is progressive tubulointerstitial fibrosis. ...
... Recent studies have shown that β-glucan in PBW can decrease systemic inflammation. This is achieved by reducing the production of leukocyte superoxide and tumor necrosis factor alpha (TNFα), as well as dampening the stimulation of interferon gene expression (Arcidiacono et al., 2019). Shanshan et al., 2019 showed that Reduning Injection had anti-inflammatory activity by inhibiting the overexpression of mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and p65 nuclear factor-κB affecting cytokine levels in COVID-19 patients (Jia et al., 2021). ...
... In addition, in cultured myoblast chemically induced hyperphosphatemia promoted cellular www.nature.com/scientificreports/ senescence, reduced their proliferative capacity and impaired myogenic differentiation indicating a possible mechanism involved in the development of sarcopenia 54 . CRP levels were found to be significantly higher in the Asiatic black bears in comparison with wild freeranging brown bears, which suggests ongoing inflammatory/infectious processes in the bile-farmed individuals 30 . ...
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... GATA6 mutations lead to a variety of cardiac phenotypes ranging from structural malformations to conduction defects (21,22). GATA6 mutations have been associated with familial BAV (23), but have been mostly found in sporadic cases (24,25). The phenotypes of mice lacking Gata6 highlight essential roles in organismal development. ...
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