Aims: Myocardial infarction (MI) remains the commonest cause of cardiac-related death throughout the world. Adverse cardiac remodelling and progressive heart failure after MI are associated with excessive and continuous damage of the extracellular matrix (ECM). In this study, we hypothesized that implantation of hydrogel into infarcted myocardium could replace the damaged ECM, thicken the infarcted wall, and inhibit cardiac remodelling. Methods and results: MI was induced in rabbits by coronary artery ligation; 4 days later, 200 µL Dex-PCL-HEMA/PNIPAAm gel solution was injected into the infarcted myocardium. Injection of phosphate-buffered saline served as control. Thirty days after treatment, histological analysis indicated that injection of the biomaterial prevented scar expansion and wall thinning compared with controls. Echocardiography studies showed that injection of hydrogel increased left ventricular ejection fraction and attenuated left ventricular systolic and diastolic dilatation. Haemodynamic analysis demonstrated improved cardiac function following implantation of the hydrogel. Conclusion: These results suggest that injection of thermosensitive Dex-PCL-HEMA/PNIPAAm hydrogel is an effective strategy that prevents adverse cardiac remodelling and dysfunction in MI rabbits.

Cardiac fibroblast (CF) proliferation and transformation into myofibroblasts play important roles in cardiac fibrosis during pathological myocardial remodeling. In this study, we demonstrate that hepatocyte growth factor (HGF), an antifibrotic factor in the process of pulmonary, renal and liver fibrosis, is a negative regulator of cardiac fibroblast transformation in response to transforming growth factor‑β1 (TGF‑β1). HGF expression levels were significantly reduced in the CFs following treatment with 5 ng/ml TGF‑β1 for 48 h. The overexpression of HGF suppressed the proliferation, transformation and the secretory function of the CFs following treatment with TGF‑β1, as indicated by the attenuated expression levels of α-smooth muscle actin (α‑SMA) and collagen I and III, whereas the knockdown of HGF had the opposite effect. Mechanistically, we identified that the phosphorylation of c‑Met, Akt and total protein of TGIF was significantly inhibited by the knockdown of HGF, but was significantly enhanced by HGF overexpression. Collectively, these results indicate that HGF activates the c‑Met‑Akt‑TGIF signaling pathway, inhibiting CF proliferation and transformation in response to TGF‑β1 stimulation.

The drug-coated balloon (DCB) is an emerging percutaneous coronary intervention (PCI) device that delivers drugs to diseased vessels to decrease the rate of vascular stenosis. Recent clinical studies have demonstrated that DCBs tend to have both good safety and efficacy profiles, leading to extended application indications in the clinic, including in-stent restenosis (ISR) for metal stents such as drug-eluting stents (DESs), small vascular disease, bifurcation disease, large vascular disease, acute coronary syndrome (ACS), and high bleeding risk. However, some previous clinical data have suggested that DCBs performed less effectively than DESs. No studies or reviews have systematically discussed the improvement strategies for better DCB performance until now. Drug loss during the process of delivery to the target lesion and inefficient delivery of the coating drug to the diseased vascular wall are two key mechanisms that weaken the efficiency of DCBs. This review is the first to summarize the key influencing factors of DCB efficiency in terms of balloon structure and principles, and then it analyzes how these factors cause outcomes in practice based on current clinical trial studies of DCBs in the treatment of different types of lesions. We also provide some recommendations for improving DCBs to contribute to better DCB performance by improving the design of DCBs and combining other factors in clinical practice.