Heart failure (HF) is closely linked to endothelial dysfunction, which contributes significantly to its progression. Endothelial dysfunction in HF is marked by reduced nitric oxide bioavailability, increased oxidative stress and inflammation, all of which impair vascular function. Endothelial progenitor cells (EPCs) – vital for vascular repair – are particularly affected, with their dysfunction further exacerbating HF outcomes. Emerging therapies targeting these mechanisms, including antioxidants, gene therapies enhancing endothelial nitric oxide synthase activity and EPC-based strategies, hold promise. Recent advances show encouraging results, especially with treatments improving EPC mobilisation and function. Additionally, pharmacological agents such as statins and sodium–glucose cotransporter 2 inhibitors demonstrate pleiotropic benefits, enhancing endothelial health and EPC activity. This review emphasises the therapeutic potential of these approaches, highlighting the critical need for further research to optimise endothelial-targeted treatments and improve outcomes for HF patients.
Carulli et al. (Mon,) studied this question.
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