Fig 1: eCCr and serum CysC of total study patients, including patients with different renal functions classified by CKD staging. (A) With decreased renal function, the serum CysC increased across CKD stages in both the HBP and non-HBP groups; (B) across the total cases, serum CysC was higher in patients with hypertension (1.07±0.30 vs. 1.00±0.27 mg/L, P<0.01) and eCCr was lower in patients with hypertension (83.89±18.69 vs. 87.95±17.04 mL/min/1.73 m2, P<0.01). In CKD stage 1 patients, serum CysC was higher (0.93±0.13 vs. 0.89±0.13 mg/L, P<0.01) in patients with hypertension, while no statistically significant difference in eCCr was found between groups. In CKD stage 2–4 patients, there was no statistically significant difference in serum CysC between the two groups. CKD, chronic kidney disease; eCCr, endogenous creatinine clearance rate; HBP, hypertension; CysC, cystatin C.
Fig 2: Effects of CysC on the development of myocardial hypertrophy in rat primary cardiomyocytes. (A) Immunofluorescence staining of α-actinin in primary cardiomyocytes and measurement of cross-sectional area; (B) MAPK phosphorylation of primary cardiomyocytes after intervention with CysC (500 ng/mL) at different time points; (C) ERK and TAK1 phosphorylation of primary cardiomyocytes after 10-minute intervention with CysC of different concentrations; (D) gene expression of Nppa, Nppb, and Myh7 of primary cardiomyocytes after 6-hour intervention with CysC of different concentrations (*, P<0.05; **, P<0.01). ERK, extracellular regulated protein kinase; JNK, c-Jun N-terminal kinase; TAK1, transforming growth factor activated kinase-1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; CysC, cystatin C.
Fig 3: Changes in CysC levels in the myocardium of TAC mice. (A) C57BL/6 wild type mouse heart echocardiogram and left ventricular pressure (LVESP and LVEDP) 14 and 28 days after TAC; (B) CysC levels in TAC mouse myocardium (*, P<0.05; **, P<0.01). TAC, transverse aortic constriction; LVEDP, left ventricular end-diastolic pressure; LVESP, left ventricular end-systolic pressure; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.
Fig 4: Difference between LVH and non-LVH groups in hypertensive patients with CKD stage 1 and 2 without heart failure. SBP and NT-proBNP were higher in the LVH group (P<0.01). There was no statistically significant difference in eCCr between the two groups, while serum CysC was higher in the LVH group (1.02±0.17 vs. 0.98±0.16 mg/L, P<0.01). In terms of echocardiographic parameters, the LVH group showed increased LADi and LVMi (P<0.01) and decreased LVEF (P<0.05). SBP, systolic blood pressure; NT-proBNP, N terminal pro B type natriuretic peptide; eCCr, endogenous creatinine clearance rate; LVMi, left ventricular mass index; LADi, left atrial diameter index; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; CKD, chronic kidney disease; CysC, cystatin C.
Fig 5: Levels of CysC protein in cardiomyocytes and in supernatants after exogenous CysC intervention. (A) Gene expression of CST3 and GAPDH in primary cardiomyocytes after 24-hour interference of CST3-siRNA or GAPDH-siRNA; (B) CysC content in primary cardiomyocytes (cell-CysC) and in supernatants (SP-CysC) after 24-hour interference of CST3-siRNA, followed by AngII 10−6 M intervention; (C) CysC levels in primary cardiomyocytes and in supernatants after 24-hour interference of CST3-siRNA, followed by exogenous CysC intervention. AngII, Angiotensin II; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; CysC, cystatin C; SP, supernatant.
Supplier Page from Enzo Life Sciences, Inc. for Cystatin C (human), (purified)