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Background  Type 4 cardiorenal syndrome ( CRS ) refers to the cardiac injury induced by chronic kidney disease. We aimed to assess oxidative stress and cardiac injury in patients with type 4  CRS , determine whether the antioxidant apocynin attenuated cardiac injury in rats with type 4  CRS , and explore potential mechanisms.    Methods and Results  A cross‐sectional study was conducted among patients with type 4  CRS  (n=17) and controls (n=16). Compared with controls, patients with type 4  CRS  showed elevated oxidative stress, which was significantly correlated with cardiac hypertrophy and decreased ejection fraction. In vivo study, male Sprague‐Dawley rats underwent 5/6 subtotal nephrectomy and sham surgery, followed with apocynin or vehicle treatment for 8 weeks. Eight weeks after surgery, the 5/6 subtotal nephrectomy rats mimicked type 4  CRS , showing increased serum creatinine, cardiac hypertrophy and fibrosis, and decreased ejection fraction compared with sham‐operated animals. Cardiac malondialdehyde,  NADPH  oxidase activity, fibroblast growth factor‐2, and extracellular signal‐regulated kinase 1/2 (ERK1/2) phosphorylation increased significantly in the 5/6 subtotal nephrectomy rats. These changes were significantly attenuated by apocynin. In vitro study showed that apocynin reduced angiotensin  II –induced  NADPH  oxidase–dependent oxidative stress, upregulation of fibroblast growth factor‐2 and fibrosis biomarkers, and  ERK 1/2 phosphorylation in cardiac fibroblasts. Importantly, the  ERK 1/2 inhibitor U0126 reduced the upregulation of fibroblast growth factor‐2 and fibrosis biomarkers in angiotensin  II –treated fibroblasts.    Conclusions  Oxidative stress is a candidate mediator for type 4  CRS . Apocynin attenuated cardiac injury in type 4  CRS  rats via inhibiting  NADPH  oxidase–dependent oxidative stress‐activated  ERK 1/2 pathway and subsequent fibroblast growth factor‐2 upregulation. Our study added evidence to the beneficial effect of apocynin in type 4  CRS .

Apocynin Attenuates Cardiac Injury in Type 4 Cardiorenal Syndrome via Suppressing Cardiac Fibroblast Growth Factor‐2 With Oxidative Stress Inhibition