Fig. 1 | Nature Communications

Fig. 1

From: Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis

Fig. 1

Circulating miR-103a-3p is upregulated in hypertensive nephropathy patients and AngII-treated mice. ac Albumin/creatinine ratio (ACR) (a), serum miR-103a-3p levels (b), and ratio for urinary miR-103a-3p levels to the volume of 24 h urine (c) of hypertensive nephropathy (HN) patients (n = 31) and healthy controls (n = 18). *p< 0.05 relative to healthy controls (Student’s t-test). d, e Correlation between ACR and the ratio for urinary miR-103a-3p levels to the volume of 24 h urine (d) or serum miR-103a-3p levels (e) in healthy individuals and HN patients. fk Albumin excretion rates (f), ACR (g), systolic blood pressure (SBP) (h), ratio for urinary miR-103a-3p levels to the volume of 24 h urine (i), and serum miR-103a-3p levels (j) in wild-type mice (n = 8) infused with vehicle (Veh) or AngII (0.2 or 1 mg kg−1 d−1) for 4 weeks. Urinary and serum miR-103a-3p levels were analyzed by qRT-PCR. *p < 0.05, relative to vehicle control. Statistical analysis was carried out with one-way analysis of variance. k Correlation between circulating miR-103a-3p levels and ACR in vehicle- or AngII-infused mice. Data are mean ± SEM. Each symbol represents an individual sample. The corresponding source data are available in the Source Data file

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