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Hyponatremia at admission is predictive of poor prognosis in patients with acute decompensated heart failure (ADHF). We performed a meta-analysis of cohort studies to evaluate whether improvement of hyponatremia is associated with improved survival in patients with ADHF and hyponatremia. Relevant studies were identified through systematic search of PubMed and Embase. A random-effect model was used to pool the results. Predefined subgroup analyses were performed to explore the source of heterogeneity. Five thousand seven hundred fourteen patients with ADHF and hyponatremia from eight cohort studies were included. Results showed that improvement of hyponatremia during hospitalization was associated with lower risk of all-cause mortality (RR = 0.65, 95% CI 0.53 to 0.80, p < 0.001) as compared with those without improvement of hyponatremia. Results of subgroup analyses indicated that improvement of hyponatremia was associated with more remarkable changes of short-term (within 3 months after discharge) mortality (RR = 0.54) as compared with long-term mortality (RR = 0.74). Other factors such as study design, sample size, and heart failure subtypes did not affect the association. This was further confirmed by the meta-analysis of studies with multivariate analysis, which also suggested an association between improved hyponatremia and lower risk of all-cause mortality in ADHF patients (adjusted RR = 0.63, 95% CI 0.43 to 0.92, p = 0.02; I2 = 63%). These results suggested that improvement of hyponatremia in ADHF patients is associated with lower mortality risk during follow-up, particularly for the short-term mortality.

Resveratrol, a natural product, has been revealed to exert antitumor effects in multiple types of tumors. However, the antitumor effects of resveratrol on hepatocellular carcinoma (HCC) and its potential underlying mechanisms have not yet been elucidated. The present study demonstrated that resveratrol inhibited viability, proliferation, invasion and migration of HCC cells significantly in a time‑ and dose‑dependent manner, indicating that resveratrol exerted antitumor effects in HCC. Furthermore, relative expression of autophagy‑related proteins Beclin1 and LC3 II/I ratio was increased while p62 expression was decreased by resveratrol treatment dose‑dependently. The LC3+ puncta formation, which represented autophagosome formation was also markedly dose‑dependently upregulated by resveratrol treatment, suggesting that resveratrol induced autophagy in HCC cells. In addition, treatment with autophagy inhibitor 3‑methyladenine (3‑MA) counteracted the inhibitory effect of resveratrol on HCC cell proliferation, invasion and migration, indicating that suppressing autophagy may hamper the antitumor effect of resveratrol in HCC. It was revealed that resveratrol upregulated the expression of p53 while decreasing the ratio of phosphorylated protein kinase B (p‑Akt)/Akt in HCC cells. Treatment with p53 inhibitor pifithrin‑α and Akt activator insulin‑like growth factor‑1 decreased the expression of Beclin1 while significantly promoting cell proliferation, invasion and migration compared with the resveratrol treatment group. Taken together, the results of the present study revealed that resveratrol inhibited the proliferation and mobility of HCC cells through inducing autophagy via activating p53 and inhibiting phosphoinositide 3‑kinase/Akt. Enhancing autophagy can augment the antitumor effects of resveratrol in HCC. Therefore, combining resveratrol with an autophagy inducer may be a viable option for treating HCC.