RESUMEN
BACKGROUND: Recent studies have suggested a renal protective effect of coffee consumption against development of chronic kidney disease (CKD), although the results remain inconclusive. We performed a protocol for systematic review and meta-analysis to comprehensively investigate this association by summarizing all available data. METHODS: An all-round retrieval will be performed in 5 electronic journal databases from their inception to June 2021, which comprise Medline, PubMed, Embase, ScienceDirect, and the Cochrane Library. The following key words were used on combination with Boolean operators AND or OR: "coffee," "caffeine," "renal insufficiency," "chronic kidney diseases," "chronic renal diseases." Two authors completed the quality assessment using the Newcastle-Ottawa Scale for observational studies. The meta-analysis was conducted using Review Manager 5.3 software from the Cochrane Collaboration (London, UK). RESULTS: The findings of this study will be submitted to peer-reviewed journals for publication. CONCLUSION: Coffee consumption may be associated with a lower risk of incident CKD.
Asunto(s)
Cafeína/farmacología , Protocolos Clínicos , Café/metabolismo , Insuficiencia Renal Crónica/prevención & control , Cafeína/metabolismo , Cafeína/uso terapéutico , Humanos , Metaanálisis como Asunto , Insuficiencia Renal Crónica/epidemiología , Factores de Riesgo , Revisiones Sistemáticas como AsuntoRESUMEN
Store-operated calcium entry (SOCE) is pivotal in maintaining intracellular Ca2+ level and cell function; however, its role in obesity development remains largely unknown. Here, we show that the stromal interaction molecule 1 (Stim1), an endoplasmic reticulum (ER) Ca2+ sensor for SOCE, is critically involved in obesity development. Pharmacological blockade of SOCE in the brain, or disruption of Stim1 in hypothalamic agouti-related peptide (AgRP)-producing neurons (ASKO), significantly ameliorates dietary obesity and its associated metabolic disorders. Conversely, constitutive activation of Stim1 in AgRP neurons leads to an obesity-like phenotype. We show that the blockade of SOCE suppresses general translation in neuronal cells via the 2',5'-oligoadenylate synthetase 3 (Oas3)-RNase L signaling. While Oas3 overexpression in AgRP neurons protects mice against dietary obesity, deactivation of RNase L in these neurons significantly abolishes the effect of ASKO. These findings highlight an important role of Stim1 and SOCE in the development of obesity.