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1.
Respir Res ; 21(1): 83, 2020 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-32293449

RESUMEN

BACKGROUND: The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in China has been declared a public health emergency of international concern. The cardiac injury is a common condition among the hospitalized patients with COVID-19. However, whether N terminal pro B type natriuretic peptide (NT-proBNP) predicted outcome of severe COVID-19 patients was unknown. METHODS: The study initially enrolled 102 patients with severe COVID-19 from a continuous sample. After screening out the ineligible cases, 54 patients were analyzed in this study. The primary outcome was in-hospital death defined as the case fatality rate. Research information and following-up data were obtained from their medical records. RESULTS: The best cut-off value of NT-proBNP for predicting in-hospital death was 88.64 pg/mL with the sensitivity for 100% and the specificity for 66.67%. Patients with high NT-proBNP values (> 88.64 pg/mL) had a significantly increased risk of death during the days of following-up compared with those with low values (≤88.64 pg/mL). After adjustment for potential risk factors, NT-proBNP was independently correlated with in-hospital death. CONCLUSION: NT-proBNP might be an independent risk factor for in-hospital death in patients with severe COVID-19. TRIAL REGISTRATION: ClinicalTrials, NCT04292964. Registered 03 March 2020.


Asunto(s)
Infecciones por Coronavirus , Mortalidad Hospitalaria , Péptido Natriurético Encefálico/análisis , Pandemias , Fragmentos de Péptidos/análisis , Neumonía Viral , Adulto , Anciano , Betacoronavirus , COVID-19 , Prueba de COVID-19 , Técnicas de Laboratorio Clínico , Infecciones por Coronavirus/diagnóstico , Infecciones por Coronavirus/mortalidad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Mortalidad , Neumonía Viral/diagnóstico , Neumonía Viral/mortalidad , Valor Predictivo de las Pruebas , Pronóstico , Valores de Referencia , Estudios Retrospectivos , Factores de Riesgo , SARS-CoV-2
2.
Cell Death Dis ; 11(1): 44, 2020 01 22.
Artículo en Inglés | MEDLINE | ID: mdl-31969558

RESUMEN

Tissue nonspecific alkaline phosphatase (TNAP) is expressed widely in different tissues, modulating functions of metabolism and inflammation. However, the effect of TNAP on cardiac fibrosis remains controversial and needs to be further studied. The present study aims to investigate the role of TNAP on myocardial infarction (MI)-induced fibrosis and its mechanism. TNAP was upregulated in patients with MI, both in serum and injured hearts, and predicted in-hospital mortality. TNAP was also significantly upregulated after MI in rats, mostly in the border zone of the infarcted hearts combined with collagen synthesis. Administration of TNAP inhibitor, tetramisole, markedly improved cardiac function and fibrosis after MI. In the primary cultures of neonatal rat cardiac fibroblasts (CFs), TNAP inhibition significantly attenuated migration, differentiation, and expression of collagen-related genes. The TGF-ß1/Smads signaling suppression, and p-AMPK and p53 upregulation were involved in the process. When p53 inhibitor was administered, the antifibrotic effect of TNAP inhibition can be blocked. This study provides a direct evidence that inhibition of TNAP might be a novel regulator in cardiac fibrosis and exert an antifibrotic effect mainly through AMPK-TGF-ß1/Smads and p53 signals.


Asunto(s)
Fosfatasa Alcalina/metabolismo , Proteínas de la Membrana/metabolismo , Miocardio/enzimología , Miocardio/patología , Transducción de Señal , Proteínas Smad/metabolismo , Factor de Crecimiento Transformador beta1/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Adenilato Quinasa/metabolismo , Fosfatasa Alcalina/antagonistas & inhibidores , Fosfatasa Alcalina/sangre , Fosfatasa Alcalina/genética , Animales , Diferenciación Celular , Hipoxia de la Célula/efectos de los fármacos , Colágeno/metabolismo , Ciclina E/metabolismo , Fibroblastos/patología , Fibrosis , Mortalidad Hospitalaria , Humanos , Masculino , Proteínas de la Membrana/antagonistas & inhibidores , Proteínas de la Membrana/sangre , Proteínas de la Membrana/genética , Infarto del Miocardio/sangre , Infarto del Miocardio/mortalidad , Infarto del Miocardio/patología , Infarto del Miocardio/fisiopatología , Fosforilación , Ratas Sprague-Dawley , Regulación hacia Arriba/genética , Remodelación Vascular
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