Examinando por Autor "Rojas-Quintero, Joselyn"
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Ítem Alzheimer’s disease and type 2 diabetes mellitus: Pathophysiologic and pharmacotherapeutics links(Baishideng Publishing Group Inc, 2021) Rojas, Milagros; Chávez-Castillo, Mervin; Ba, Jordan; Ortega, Ángel; Nava, Manuel; Salazar, Juan; Díaz-Camargo, Edgar; Rojas-Quintero, Joselyn; Bermúdez, ValmoreAt present, Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2DM) are two highly prevalent disorders worldwide, especially among elderly individuals. T2DM appears to be associated with cognitive dysfunction, with a higher risk of developing neurocognitive disorders, including AD. These diseases have been observed to share various pathophysiological mechanisms, including alterations in insulin signaling, defects in glucose transporters (GLUTs), and mitochondrial dysfunctions in the brain. Therefore, the aim of this review is to summarize the current knowledge regarding the molecular mechanisms implicated in the association of these pathologies as well as recent therapeutic alternatives. In this context, the hyperphosphorylation of tau and the formation of neurofibrillary tangles have been associated with the dysfunction of the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in the nervous tissues as well as the decrease in the expression of GLUT-1 and GLUT-3 in the different areas of the brain, increase in reactive oxygen species, and production of mitochondrial alterations that occur in T2DM. These findings have contributed to the implementation of overlapping pharmacological interventions based on the use of insulin and antidiabetic drugs, or, more recently, azeliragon, amylin, among others, which have shown possible beneficial effects in diabetic patients diagnosed with AD.Ítem Depression as a Neuroendocrine Disorder: Emerging Neuropsychopharmacological Approaches beyond Monoamines(Hindawi, 2019) Chávez-Castillo, Mervin; Núñez, Victoria; Nava, Manuel; Ortega, Ángel; Rojas, Milagros; Bermúdez, Valmore; Rojas-Quintero, JoselynDepression is currently recognized as a crucial problem in everyday clinical practice, in light of ever-increasing rates of prevalence, as well as disability, morbidity, and mortality related to this disorder. Currently available antidepressant drugs are notoriously problematic, with suboptimal remission rates and troubling side-effect profiles. Their mechanisms of action focus on the monoamine hypothesis for depression, which centers on the disruption of serotonergic, noradrenergic, and dopaminergic neurotransmission in the brain. Nevertheless, views on the pathophysiology of depression have evolved notably, and the comprehension of depression as a complex neuroendocrine disorder with important systemic implications has sparked interest in a myriad of novel neuropsychopharmacological approaches. Innovative pharmacological targets beyond monoamines include glutamatergic and GABAergic neurotransmission, brain-derived neurotrophic factor, various endocrine axes, as well as several neurosteroids, neuropeptides, opioids, endocannabinoids and endovanilloids. This review summarizes current knowledge on these pharmacological targets and their potential utility in the clinical management of depression.Ítem Electroconvulsive Therapy in Psychiatric Disorders: A Narrative Review Exploring Neuroendocrine–Immune Therapeutic Mechanisms and Clinical Implications(MDPI, 2022) Rojas, Milagros; Ariza, Daniela; Ortega, Ángel; Riaño-Garzón, Manuel E.; Chávez-Castillo, Mervin; Pérez, José Luis; Cudris-Torres, Lorena; Bautista, María Judith; Medina-Ortiz, Oscar; Rojas-Quintero, Joselyn; Bermúdez, ValmoreElectroconvulsive therapy (ECT) is based on conducting an electrical current through the brain to stimulate it and trigger generalized convulsion activity with therapeutic ends. Due to the efficient use of ECT during the last years, interest in the molecular bases involved in its mechanism of action has increased. Therefore, different hypotheses have emerged. In this context, the goal of this review is to describe the neurobiological, endocrine, and immune mechanisms involved in ECT and to detail its clinical efficacy in different psychiatric pathologies. This is a narrative review in which an extensive literature search was performed on the Scopus, Embase, PubMed, ISI Web of Science, and Google Scholar databases from inception to February 2022. The terms “electroconvulsive therapy”, “neurobiological effects of electroconvulsive therapy”, “molecular mechanisms in electroconvulsive therapy”, and “psychiatric disorders” were among the keywords used in the search. The mechanisms of action of ECT include neurobiological function modifications and endocrine and immune changes that take place after ECT. Among these, the decrease in neural network hyperconnectivity, neuroinflammation reduction, neurogenesis promotion, modulation of different monoaminergic systems, and hypothalamus–hypophysis–adrenal and hypothalamus–hypophysis–thyroid axes normalization have been described. The majority of these elements are physiopathological components and therapeutic targets in different mental illnesses. Likewise, the use of ECT has recently expanded, with evidence of its use for other pathologies, such as Parkinson’s disease psychosis, malignant neuroleptic syndrome, post-traumatic stress disorder, and obsessive–compulsive disorder. In conclusion, there is sufficient evidence to support the efficacy of ECT in the treatment of different psychiatric disorders, potentially through immune, endocrine, and neurobiological systems.Ítem Neprilysin: A Potential Therapeutic Target of Arterial Hypertension?(Bentham Science Publishers, 2020) Salazar, Juan; Rojas-Quintero, Joselyn; Cano, Clímaco; Pérez, José L.; Ramírez, Paola; Carrasquero, Rubén; Torres, Wheeler; Espinoza, Cristobal; Chacín-González, Maricarmen; Bermúdez, ValmoreArterial hypertension is the most prevalent chronic disease in the adult population of developed countries and it constitutes a significant risk factor in the development of cardiovascular disease, contributing to the emergence of many comorbidities, among which heart failure excels, a clinical syndrome that nowadays represents a major health problem with uncountable hospitalizations and the indolent course of which progressively worsens until quality of life decreases and lastly death occurs prematurely. In the light of this growing menace, each day more efforts are invested in the field of cardiovascular pharmacology, searching for new therapeutic options that allow us to modulate the physiological systems that appear among these pathologies. Therefore, in the later years, the study of natriuretic peptides has become so relevant, which mediate beneficial effects at the cardiovascular level such as diuresis, natriuresis, and decreasing cardiac remodeling; their metabolism is mediated by neprilysin, a metalloproteinase, widely expressed in the human and capable of catalyzing many substrates. The modulation of these functions has been studied by decades, giving room to Sacubitril, the first neprilysin inhibitor, which in conjunction with an angiotensin receptor blocker has provided a high efficacy and tolerability among patients with heart failure, for whom it has already been approved and recommended. Nonetheless, in the matter of arterial hypertension, significant findings have arisen that demonstrate the potential role that it will play among the pharmacological alternatives in the upcoming years.Ítem NHANES 2011–2014 Reveals Decreased Cognitive Performance in U.S. Older Adults with Metabolic Syndrome Combinations(MDPI, 2023) Díaz-Camargo, Edgar; Hernández-Lalinde, Juan; Sánchez-Rubio, María; Chaparro-Suárez, Yudy; Álvarez-Caicedo, Liseth; Fierro-Zarate, Alexandra; Gravini-Donado, Marbel; García-Pacheco, Henry; Rojas-Quintero, Joselyn; Bermúdez, ValmoreA relationship between metabolic syndrome and cognitive impairment has been evidenced across research; however, conflicting results have been observed. A cross-sectional study was conducted on 3179 adults older than 60 from the 2011–2014 National Health and Nutrition Examination Survey (NHANES) to analyze the relationship between metabolic syndrome and cognitive impairment. In our results, we found that adults with abdominal obesity, high triglycerides, and low HDL cholesterol had 4.39 fewer points in the CERAD immediate recall test than adults without any metabolic syndrome factors [Beta = −4.39, SE = 1.32, 17.75 (1.36) vs. 22.14 (0.76)]. In addition, people with this metabolic syndrome combination exhibited 2.39 fewer points in the CERAD delayed recall test than those without metabolic syndrome criteria [Beta = −2.39, SE = 0.46, 4.32 (0.49) vs. 6.71 (0.30)]. It was also found that persons with high blood pressure, hyperglycemia, and low HDL–cholesterol levels reached 4.11 points less in the animal fluency test than people with no factors [Beta = −4.11, SE = 1.55, 12.67 (2.12) vs. 16.79 (1.35)]. These findings suggest that specific metabolic syndrome combinations are essential predictors of cognitive impairment. In this study, metabolic syndrome combinations that included obesity, fasting hyperglycemia, high triglycerides, and low HDL–cholesterol were among the most frequent criteria observed.Ítem Non-HDL cholesterol is better than LDL-c at predicting atherosclerotic cardiovascular disease risk factors clustering, even in subjects with near-to-normal triglycerides: A report from a Venezuelan population(F1000 Research Ltd., 2018-09-20) Bermúdez, Valmore; Torres, Wheeler; Salazar, Juan; Martínez, María Sofía; Rojas, Edward; Olivar, Luis Carlos; Lameda, Victor; Ortega, Ángel; Ramírez, Paola; Rojas, Milagros; Rastogi, Sheena; D’Addosio, Rosanna; Hoedebecke, Kyle; Graterol, Modesto; Graterol, Resemily; Wilches, Sandra; Cabrera de Bravo, Mayela; Rojas-Quintero, JoselynBackground: Non-high density lipoprotein cholesterol (non-HDL-c) has emerged as an important tool in primary prevention of atherosclerotic cardiovascular disease (ASCVD), especially among those at high risk. The main objective of this study was to evaluate the predictive value of non-HDL-c for the coexistence aggregation of multiple ASCVD risk factors and compare this with LDL-c in general subjects with normal or near normal triglycerides from Maracaibo city in Venezuela. Methods: This is a descriptive, cross-sectional study with a randomized multistage sampling. 2026 subjects were selected for this study, all were adults ≥18 years old of both genders and inhabitants of Maracaibo city, Venezuela. A complete history and physical medical assessment was performed. A multivariate logistic regression model was used to determine the odds ratio (CI95%) for the coexistence of multiple risk factors for ASCVD. Results: The median (p25-p75) of non-HDL-c was 143 mg/dL (114-174 mg/dL). 52.1% (n=1056) of the sample were women, with a median of 144 mg/dL (115-174 mg/dL) among women and 143 mg/dL (114-17 4mg/dL) among men; p=0.740. Individuals ≥50 years old, smokers, those with hypertension, obesity, diabetes, high waist circumference and elevated hs-C Reactive Protein, all had higher levels of non-HDL-c. A lower median was observed among those <30 years of age with elevated physical activity levels in their leisure time. Non-HDL-c between 130-159 mg/dL (OR=2.44; CI 95%=1.48-4.02; p<0.001) and ≥160 mg/dL (OR=3.28; CI 95%=1.72-6.23; p<0.001) was associated with greater risk of coexistent multiple risk factors for ASCVD, albeit LDL-c was not significant in the multivariate model. Conclusions: Elevated non-HDL-c was associated with conglomeration of multiple risk factors for ASCVD. This suggests evaluation of non-HDL-c may be of better utility in primary care for early identification of subjects for high risk of ASCVD. Future research might focus on the influence of non-HDL-c in cardiovascular mortality.Ítem The quest for immunotherapy in atherosclerosis: CANTOS study, interleukin-1β and vascular inflammation(AME Publishing Company, 2017-12) Bermúdez, Valmore; Rojas-Quintero, Joselyn; Velasco, Manuelespite the monumental efforts directed into studying and describing the pathways, factors, genetic predisposition, and target-specific pharmacotherapy to atherosclerosis, ischemic heart disease, thrombotic cerebrovascular disease and peripheral artery disease are still responsible for 50% of all the deaths occurring in the developed world. The quest for a clear pathophysiology into atherosclerosis began with von Rokitansky’s incrustation theory, which evolved into the crucial role of platelets and thrombogenesis during acute coronary syndromes (1). Next, came the irritation theory postulated by Virchow, which detailed the presence of leukocytes in atherosclerotic plaques, suggesting the presence of chronic inflammation and progressive vessel deformation (1). By 1904, the term atherosclerosis was coined by Felix Jacob Marchand and 9 years later Nikolai Anichkov published that cholesterol alone can induce the vascular changes associated with atherosclerosis (1). The impeccable work performed by Anichkov and his team, paved the way to the current understanding and clinical logic used in current cardiovascular medicine (the lipid hypothesis), which for the longest period focused mainly in plasma lipids as sole culprits for atherogenesis. Genetic connection between cholesterol and heart disease came in 1939, when Müller described families with severe hypercholesterolemia and early onset cardiac disease and death (2). The recognition of hereditary hyperlipidemias and their characteristics, cemented the role on cholesterol in cardiovascular risk, along with the findings from the epidemiological mammoth, the Framingham Heart Study (3). At some point, the lipid hypothesis was “universally recognized as a law” [2002] (4), and as such, it dominated pharmacotherapy development in cardiovascular medicine.Ítem Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review(MDPI, 2021) Cano, Raquel; Pérez, José L.; Angarita Dávila, Lissé; Ortega, Ángel; Gómez, Yosselin; Valero-Cedeño, Nereida Josefina; Parra, Heliana; Manzano, Alexander; Véliz Castro, Teresa Isabel; Díaz Albornoz, María P; Cano, Gabriel; Rojas-Quintero, Joselyn; Chacín, Maricarmen; Bermúdez, ValmoreNon-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.Ítem SGLT2i and GLP-1RA in Cardiometabolic and Renal Diseases: From Glycemic Control to Adipose Tissue Inflammation and Senescence(Hindawi, 2021) D'Marco, Luis; Morillo, Valery; Gorriz, José Luis; Suarez, María K.; Nava, Manuel; Ortega, Ángel; Parra, Heliana; Villasmil, Nelson; Rojas-Quintero, Joselyn; Bermúdez, ValmoreBackground. Over the last few years, the use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) and glucagon-like peptide 1 receptor agonists (GLP-1RA) has increased substantially in medical practice due to their documented benefits in cardiorenal and metabolic health. In this sense, and in addition to being used for glycemic control in diabetic patients, these drugs also have other favorable effects such as weight loss and lowering blood pressure, and more recently, they have been shown to have cardio and renoprotective effects with anti-inflammatory properties. Concerning the latter, the individual or associated use of these antihyperglycemic agents has been linked with a decrease in proinflammatory cytokines and with an improvement in the inflammatory profile in chronic endocrine-metabolic diseases. Hence, these drugs have been positioned as first-line therapy in the management of diabetes and its multiple comorbidities, such as obesity, which has been associated with persistent inflammatory states that induce dysfunction of the adipose tissue. Moreover, other frequent comorbidities in long-standing diabetic patients are chronic complications such as diabetic kidney disease, whose progression can be slowed by SGLT2i and/or GLP-1RA. The neuroendocrine and immunometabolism mechanisms underlying adipose tissue inflammation in individuals with diabetes and cardiometabolic and renal diseases are complex and not fully understood. Summary. This review intends to expose the probable molecular mechanisms and compile evidence of the synergistic or additive anti-inflammatory effects of SGLT2i and GLP-1RA and their potential impact on the management of patients with obesity and cardiorenal compromise.