Broken signals: when the mineralostat alters the cardiovascular system

Patients with kidney disease face a markedly increased risk of developing cardiovascular disease (CVD) which manifests in multiple forms, including: left ventricular hypertrophy, heart failure, atherosclerosis, and vascular inflammation, all of which are associated in clinical studies to well-characterized morbidity and mortality reported throughout disease progression. These patients also exhibit disturbances in mineral metabolism and in the network of signals that regulate mineral balance, that we collectively refer to as the "mineralostat." This review aims to summarize the links between mineralostat alterations and its potential implications for the onset and progression of CVD, as disruptive signals are transmitted to the heart and vascular system. Over the past decade, studies using sophisticated preclinical models have identified new proteins and signaling pathways of the mineralostat as candidates contributing to CVD. Here, we discuss the pathophysiological conditions reported to disrupt the mineralostat, the hormones involved in mineral metabolism, and the minerals. We also summarize the mechanisms through which each of these factors may promote CVD, with attention to their relevance for patients.