BackgroundExisting evidence on the association between blood pressure (BP) and mortality risk in intensive care unit (ICU) patients with atrial fibrillation (AF) is scarce.AimThis study aimed to assess the associations between blood pressure (BP) and risks of in-hospital and all-cause mortality in ICU patients with AF.MethodsA total of 2,345 records of patients with AF whose BP was monitored after admission to the ICU were obtained from the MIMIC-III database. Incidences were calculated for endpoints (hospital mortality, 7-day mortality, 30-day mortality, and 1-year mortality). We performed smooth curve and logistic regression analyses to evaluate the association between BP and the risk of each endpoint.ResultsSmooth curve regression showed that systolic blood pressure (SBP), mean arterial pressure (MBP), and diastolic blood pressure (DBP) followed U-shaped curves with respect to endpoints (hospital mortality, 7-day mortality, 30-day mortality, and 1-year mortality). The incidence of these endpoints was lowest at 110/70/55 mm Hg. There was an increased risk of 1-year mortality observed with BP > 110/70/55 mm Hg (SBP, odds ratio [OR] = 1.008, 95% CI 1.001–1.015, p = 0.0022; MBP, OR = 1.010, 95% CI 1.005–1.016, p < 0.001) after adjusting for age, sex, and medical history. In contrast, an inverse association between BP and the risk of 1-year mortality was observed with BP ≤ 110/70/55 mm Hg (SBP, OR = 0.981, 95% CI 0.974–0.988, p < 0.001; MBP OR = 0.959, 95% CI 0.939–0.979, p < 0.001; and DBP, OR = 0.970, 95% CI 0.957–0.983, p < 0.001).ConclusionsWe observed a U-shaped association between BP and in-hospital/all-cause mortality in ICU patients with AF. However, the underlying causes need to be investigated.

Renal fibrosis is the pathological hallmark of chronic kidney disease that is influenced by numerous factors. Arrest of renal tubular epithelial cells (RTECs) in G2/M phase is closely correlated with the progression of renal fibrosis; however, the mechanisms mediating these responses remain poorly defined. In this study, we observed that human leukocyte antigen-F adjacent transcript 10 (FAT10) deficiency abolished hypoxia-induced upregulation of checkpoint kinase 1 (CHK1) expression in RTECs derived from FAT10 +/+ and FAT10 −/− mice. Further investigations revealed that FAT10 contributes to CHK1-mediated G2/M arrest and production of pro-fibrotic cytokines in RTECs exposed to hypoxia. Mechanistically, FAT10 directly interacted with and stabilized the deubiquitylating enzyme ubiquitin specific protease 7 (USP7) to mediate CHK1 upregulation, thereby promoting CHK1-mediated G2/M arrest in RTECs. In animal model, FAT10 expression was upregulated in the obstructed kidneys of mice induced by unilateral ureteric obstruction injury, and FAT10 −/− mice exhibited reduced unilateral ureteric obstruction injury induced-renal fibrosis compared with FAT10 +/+ mice. Furthermore, in a cohort of patients with calculi-related chronic kidney disease, upregulated FAT10 expression was positively correlated with renal fibrosis and the USP7/CHK1 axis. These novel findings indicate that FAT10 prolongs CHK1-mediated G2/M arrest via USP7 to promote renal fibrosis, and inhibition of the FAT10/USP7/CHK1 axis might be a plausible therapeutic approach to alleviate renal fibrosis in chronic kidney disease.