Mechanisms by which iron deficiency affects cardiovascular diseases and advances in therapeutic strategies

HE Peng-yuan; SHEN Xiang-li; JIANG Shu-bin

doi:10.13820/j.cnki.gdyx.20252143

Abstract：Iron deficiency is a highly prevalent comorbidity in patients with heart failure and has gained increasing recognition as an independent determinant of disease severity,functional impairment,and adverse clinical outcomes,irre-spective of the presence of anemia.Accumulating evidence indicates that iron deficiency contributes to heart failure pro-gression through multiple pathophysiological pathways,including impaired myocardial energy metabolism,mitochondrial dysfunction,increased oxidative stress,inflammatory activation,and maladaptive cardiac remodeling.At the cellular lev-el,insufficient iron availability compromises oxidative phosphorylation and ATP generation,thereby reducing myocardial contractile efficiency and exercise capacity.Clinically,iron deficiency has been consistently associated with reduced quali-ty of life,diminished functional status,and higher risks of hospitalization in patients with both heart failure with reduced and preserved ejection fraction.Over the past decade,randomized controlled trials have demonstrated that intravenous iron supplementation can significantly improve symptoms,exercise tolerance,and health-related quality of life in iron-defi-cient heart failure patients,even in the absence of anemia.Although the impact of iron repletion on long-term mortality remains under active investigation,current evidence supports routine screening and targeted treatment of iron deficiency as an integral component of comprehensive heart failure management.Continued research is warranted to refine patient selec-tion,optimize therapeutic strategies,and elucidate the long-term prognostic benefits of iron correction in heart failure.