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Currently, cardiovascular diseases are a major contributor to morbidity and mortality worldwide, having a significant negative impact on both the economy and public health. The renin-angiotensin system contributes to a high spectrum of cardiovascular disorders and is essential for maintaining normal cardiovascular homeostasis. Overactivation of the classical renin-angiotensin system is one of the most important pathophysiological mechanisms in the progression of cardiovascular diseases. The counter-regulatory renin-angiotensin system is an alternate pathway which favors the synthesis of different peptides, including Angiotensin-(1-7), Angiotensin-(1-9), and Alamandine. These peptides, via the angiotensin type 2 receptor (AT2R), MasR, and MrgD, initiate multiple downstream signaling pathways that culminate in the activation of various cardioprotective mechanisms, such as decreased cardiac fibrosis, decreased myocardial hypertrophy, vasodilation, decreased blood pressure, natriuresis, and nitric oxide synthesis. These cardioprotective effects position them as therapeutic alternatives for reducing the progression of cardiovascular diseases. This review aims to show the latest findings on the cardioprotective effects of the main peptides of the counter-regulatory renin-angiotensin system.
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The use of cardioprotective strategies as adjuvants of cardioplegic solutions has become an ideal alternative for the improvement of post-surgery heart recovery. The choice of the optimal cardioplegia, as well as its distribution mechanism, remains controversial in the field of cardiovascular surgery. There is still a need to search for new and better cardioprotective methods during cardioplegic procedures. New techniques for the management of cardiovascular complications during cardioplegia have evolved with new alternatives and additives, and each new strategy provides a tool to neutralize the damage after ischemia/reperfusion events. Researchers and clinicians have committed themselves to studying the effect of new strategies and adjuvant components with the potential to improve the cardioprotective effect of cardioplegic solutions in preventing myocardial ischemia/reperfusion-induced injury during cardiac surgery. The aim of this review is to explore the different types of cardioplegia, their protection mechanisms, and which strategies have been proposed to enhance the function of these solutions in hearts exposed to cardiovascular pathologies that require surgical alternatives for their corrective progression.
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OBJECTIVE: To define the relationship between chronic chikungunya post-viral arthritis disease severity, cytokine response and T cell subsets in order to identify potential targets for therapy. METHODS: Participants with chikungunya arthritis were recruited from Colombia from 2019-2021. Arthritis disease severity was quantified using the Disease Activity Score-28 and an Arthritis-Flare Questionnaire adapted for chikungunya arthritis. Plasma cytokine concentrations (interleukin (IL)-1ß, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, interferon-γ and tumor necrosis factor (TNF)) were measured using a Meso Scale Diagnostics assay. Peripheral blood T cell subsets were measured using flow cytometry. RESULTS: Among participants with chikungunya arthritis (N = 158), IL-2 levels and frequency of regulatory T cells (Tregs) were low. Increased arthritis disease activity was associated with higher levels of inflammatory cytokines (IL-6, TNF and CRP) and immunoregulatory cytokine IL-10 (p<0.05). Increased arthritis flare activity was associated with higher Treg frequencies (p<0.05) without affecting T effector (Teff) frequencies, Treg/Teff ratios and Treg subsets. Finally, elevated levels of IL-2 were correlated with increased Treg frequency, percent Tregs out of CD4+ T cells, and Treg subsets expressing immunosuppressive markers, while also correlating with an increased percent Teff out of live lymphocytes (p<0.05). CONCLUSION: Chikungunya arthritis is characterized by increased inflammatory cytokines and deficient IL-2 and Treg responses. Greater levels of IL-2 were associated with improved Treg numbers and immunosuppressive markers. Future research may consider targeting these pathways for therapy.
Assuntos
Artrite Infecciosa , Febre de Chikungunya , Humanos , Citocinas/metabolismo , Interleucina-10/metabolismo , Estudos Transversais , Interleucina-2/metabolismo , Interleucina-6/metabolismo , Febre de Chikungunya/complicações , Linfócitos T Reguladores/metabolismo , Linfócitos T CD4-Positivos/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , ImunossupressoresRESUMO
Las sibilancias se definen como sonidos pulmonares adventicios, continuos y de tono alto. Predominantemente las sibilancias son de naturaleza espiratoria, pero también pueden ser inspiratorias o bifásicas. Su etiología es secundaria a la obstrucción de flujo en vía aérea superior extratorácica, vía aérea superior intratorácica o vía aérea inferior. Se cree que las sibilancias se deben a las vibraciones de las paredes de las vías respiratorias ocluidas, inducidas por una velocidad reducida del flujo de aire. Cuando se perciben sibilancias sin inducir exhalación forzada es necesario estudiar la causa, realizando una historia clínica dirigida a las diversas etiologías y un examen físico que incluya la exploración torácica completa: inspección, palpación, percusión y auscultación. Ayudas diagnósticas como la radiografía de tórax, la espirometría pre y posbroncodilatador, la tomografía computarizada de tórax y la broncoscopia pueden ser necesarias. El objetivo de este artículo es demostrar que las sibilancias representan un hallazgo semiológico retador para el clínico, que obliga no solo a pensar en asma o en enfermedad pulmonar obstructiva crónica (EPOC) como posible causa.
Wheezing is defined as adventitious, continuous and high-tone lung sounds. Predominantly the wheezing is of an expiratory nature, but it can also be inspiratory or biphasic. Its etiology is secondary to flow obstruction in the extrathoracic and intrathoracic upper airway, or lower airway. It is believed that wheezing is due to vibrations of the walls of the occluded airways, induced by a reduced speed of air flow. When wheezing is perceived without inducing forced exhalation, it is necessary to study the cause, perform a medical history directed at the various etiologies and a physical health check that includes complete chest examination: Inspection, palpation, percussion, and auscultation. As diagnostic aids like chest x-ray, pre- and post-bronchodilator spirometry, computed tomography of the chest and bronchoscopy may be necessary. The objective of this article is demonstrate that wheezing represents a challenging clinical finding for the medical doctor and suggests that it is important to consider other causes in addition to Asthma or Chronic Obstructive Pulmonary Disease (COPD).
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HumanosRESUMO
Resumen La aterosclerosis es una arteriopatía inflamatoria, crónica y progresiva que genera disfunción del endotelio vascular, estenosis y obstrucción de los vasos sanguíneos. Lidera las estadísticas relacionadas con enfermedades circulatorias y es la principal causa de cardiopatía isquémica. En el mundo representa la principal causa de muerte en la población general. Actualmente, las infecciones representan uno de los principales factores de riesgo emergentes asociados con la aterosclerosis. Varios estudios recientes han demostrado que la enfermedad periodontal está asociada a enfermedades cardiovasculares, que tienen como base la aterosclerosis; por tanto, la relación entre Porphyromonas gingivalis y aterosclerosis coronaria es un terreno activo de investigación en el ámbito global. El lipopolisacárido de la membrana externa y las gingipaínas de Porphyromonas gingivalis están vinculadas a los procesos inflamatorios que ocurren durante el proceso aterogénico. Por consiguiente, la infección periodontal producida por este microorganismo podría desencadenar mecanismos moleculares proinflamatorios involucrados en la etiopatogenia de la aterosclerosis coronaria. Esta revisión tiene como objetivo detallar, de manera minuciosa y precisa, los mecanismos celulares y moleculares implicados en la cardiopatía isquémica por ateromatosis coronaria asociada a la infección por Porphyromonas gingivalis.
Abstract Atherosclerosis is an inflammatory, chronic and progressive arteriopathy that generates vascular endothelial dysfunction with stenosis and obstruction of blood vessels. It is the main cause of circulatory diseases, especially ischemic heart disease. This pathology leads the statistics related to circulatory diseases and is the main cause of ischemic heart disease. Worldwide, atherosclerosis represents the leading cause of death in the general population. Currently, infections represent one of the main emerging risk factors associated with atherosclerosis, several recent studies have shown that periodontal disease is associated with cardiovascular diseases, based on atherosclerosis. The association between Porphyromonas gingivalis and coronary atherosclerosis is an active field of research at a global level. The outer membrane of lipopolysaccharide and the gingipains of Porphyromonas gingivalis are linked to the inflammatory processes that occur during the atherogenic process. Consequently, the periodontal infection caused by Porphyromonas gingivalis could be triggering proinflammatory molecular mechanisms involved in the etiopathogenesis of coronary atherosclerosis. This review aims to detail in a meticulous and precise way the cellular and molecular mechanisms involved in ischemic heart disease due to coronary atheromatosis associated with Porphyromonas gingivalis infection.