miR-320 accelerates chronic heart failure with cardiac fibrosis through activation of the IL6/STAT3 axis.

Cardiac fibrosis could induce abnormal cardiac function and become a novel target for cardiac hypertrophy and chronic heart failure. MiRNA-320 is a crucial miRNA in cardiovascular disease, but it is poorly understood whether it plays a role in cardiac fibrosis pathogenesis. We aimed to identify the specific underlying mechanism of miR-320 in cardiac fibrosis and hypertrophic pathogenesis. In our study, the GEO datasets revealed that STAT3 was significantly highly expressed in cardiomyocyte lines. MiR-320 activation and STAT3 signaling pathways were statistically significantly connected. Furthermore, miR-320 was highly associated with cardiac fibrosis and hypertrophic disease. Interstitial fibrosis was observed in the mice subjected to TAC surgery, markedly enhanced in miR-320 mimics. Mechanistically, we revealed that miR-320 mimics aggravated the pressure overload and induced cardiac hypertrophy and fibrosis via the IL6/STAT3/PTEN axis. MiR-320 mimics accelerated cardiac hypertrophy and cardiac fibrosis via the IL6/STAT3/PTEN axis. These results suggest that targeting miR-320 may represent a potential therapeutic strategy for cardiac hypertrophy and fibrosis.

Recombinant Brain Natriuretic Peptide for the Prevention of Contrast-Induced Nephropathy in Patients with Chronic Kidney Disease Undergoing Nonemergent Percutaneous Coronary Intervention or Coronary Angiography: A Randomized Controlled Trial.

The role of brain natriuretic peptide (BNP) in the prevention of contrast-induced nephropathy (CIN) is unknown. This study aimed to investigate BNP's effect on CIN in chronic kidney disease (CKD) patients undergoing elective percutaneous coronary intervention (PCI) or coronary angiography (CAG). The patients were randomized to BNP (0.005 µg/kg/min before contrast media (CM) exposure and saline hydration, n = 106) or saline hydration alone (n = 103). Cystatin C, serum creatinine (SCr) levels, and estimated glomerular filtration rates (eGFR) were assessed at several time points. The primary endpoint was CIN incidence; secondary endpoint included changes in cystatin C, SCr, and eGFR. CIN incidence was significantly lower in the BNP group compared to controls (6.6% versus 16.5%, P = 0.025). In addition, a more significant deterioration of eGFR, cystatin C, and SCr from 48 h to 1 week (P < 0.05) was observed in controls compared to the BNP group. Although eGFR gradually deteriorated in both groups, a faster recovery was achieved in the BNP group. Multivariate logistic regression revealed that using >100 mL of CM (odds ratio: 4.36, P = 0.004) and BNP administration (odds ratio: 0.21, P = 0.006) were independently associated with CIN. Combined with hydration, exogenous BNP administration before CM effectively decreases CIN incidence in CKD patients.

Brain natriuretic peptide for prevention of contrast-induced nephropathy after percutaneous coronary intervention or coronary angiography.

BACKGROUND: Many methods reportedly prevent contrast-induced nephropathy (CIN), but the effect of brain natriuretic peptide (BNP) on CIN is unknown. In this study we investigated recombinant BNP use before coronary angiography (CA) or nonemergent percutaneous coronary intervention (PCI) in patients with unstable angina. METHODS: One thousand patients with unstable angina were prospectively evaluated. The patients were randomly assigned to: group A, isotonic normal saline (NaCl 0.9%, 1 mL/kg/h) for 24 hours before CA or PCI; and group B, human recombinant BNP (rhBNP; 0.005 µg/kg/min). Serum creatinine (Scr) levels and estimated glomerular filtration rate were measured before and 24, 48, and 72 hours, and 7 days after the procedure. The primary outcome was CIN incidence defined according to a relative (≥ 25%) or absolute (≥ 0.5 mg/dL and 44 µmol/L, respectively) increase in Scr from baseline within 48 hours. The secondary end points were the changes in the Scr and estimated glomerular filtration rate, before and after the procedure. RESULTS: Contrast volume, a history of diabetes mellitus, and BNP administration independently predicted CIN. The incidence of CIN was significantly greater in group A than in group B (14.8% vs 5.6%; P < 0.01). Renal function was less compromised in patients who received rhBNP. The Scr of all patients with CIN remained increased for 24 hours, but it was lower and recovered faster in patients who received rhBNP. CONCLUSIONS: rhBNP administration before CA or PCI protects renal function and can significantly decrease CIN incidence.