The Ferroptosis Nexus: A New Culprit in Heart Failure Emergencies A comprehensive review in *Cardiovascular Research* synthesizes the growing evidence implicating ferroptosis—a form of iron-dependent, lipid peroxidation-driven cell death—in the progression of heart failure. The analysis spans multiple animal models, from chronic ischemic and pressure overload to septic and doxorubicin-induced cardiomyopathy, finding that disordered iron handling, antioxidant failure, and mitochondrial stress converge to trigger this lethal pathway, leading to contractile dysfunction and adverse cardiac remodeling.

Ferroptosis: A New Culprit in the Failing Heart A comprehensive review in Cardiovascular Research synthesizes the growing evidence linking ferroptosis—a form of iron-dependent, lipid peroxidation-driven cell death—to the progression of heart failure. The analysis details how this pathway is activated across diverse cardiomyopathy models, from ischemic and pressure-overloaded hearts to those damaged by metabolic disease or toxins like doxorubicin. Crucially, the review highlights that several cardiometabolic drugs with proven clinical efficacy, including SGLT2 inhibitors and sacubitril/valsartan, appear to mitigate ferroptotic activity.

The Iron Link: How a New Form of Cell Death Fuels Heart Failure A comprehensive review in Cardiovascular Research synthesizes the growing evidence linking ferroptosis—a form of iron-dependent, lipid peroxidation-driven cell death—to the progression of heart failure. The analysis finds that ferroptosis is prevalent across diverse heart failure models, including those related to ischemia, pressure overload, diabetes, and drug toxicity. The process involves a self-reinforcing "nexus" of disordered iron handling, antioxidant system collapse, and mitochondrial stress, leading to contractile dysfunction and adverse cardiac remodeling.

Ferroptosis: A Newly Recognized Culprit in Heart Failure Progression A comprehensive review in *Cardiovascular Research* synthesizes emerging evidence that ferroptosis, a form of iron-dependent programmed cell death driven by lipid peroxidation, is a significant contributor to heart failure. The analysis spans multiple animal models—including those for ischemic, pressure overload, and diabetic cardiomyopathy—and finds that dysregulated iron metabolism, antioxidant system failure, and mitochondrial stress converge to trigger this cell death pathway, leading to contractile dysfunction and adverse cardiac remodeling.

The Iron Link: How a Novel Cell Death Pathway Fuels Chronic Inflammation A comprehensive review in Cardiovascular Research synthesizes evidence for ferroptosis—a form of iron-dependent, lipid peroxidation-driven cell death—as a significant contributor to heart failure progression. The analysis details how dysregulated iron metabolism, antioxidant system failure, and mitochondrial stress converge to trigger this process across multiple disease models. Notably, the review proposes a "ferroptosis nexus" framework and highlights that several existing cardiometabolic drugs, including SGLT2 inhibitors, appear to modulate this pathway, offering a mechanistic explanation for their clinical benefits beyond their primary indications.

The Iron Heart: How a New Form of Cell Death Fuels Heart Failure A comprehensive review in *Cardiovascular Research* synthesizes the growing evidence for ferroptosis—a form of iron-dependent, lipid peroxidation-driven cell death—as a central mechanism in heart failure progression. The analysis shows ferroptosis is abundant in the myocardium across diverse heart failure models, from chronic ischemic and pressure overload to septic and doxorubicin-induced cardiomyopathy.

A new nexus for heart failure: iron, lipids, and cell death A comprehensive review synthesizes evidence that ferroptosis, a form of iron-dependent cell death driven by lipid peroxidation, is a prominent feature in the failing heart across multiple animal models, including those for ischemic, pressure overload, and diabetic cardiomyopathy. The authors propose a "ferroptosis nexus" model where dysregulated iron handling, antioxidant failure, and mitochondrial stress create a self-reinforcing loop leading to pump dysfunction.

A New Nexus: How Iron-Driven Cell Death Fuels Heart Failure and Kidney Risk A comprehensive review in Cardiovascular Research synthesizes the growing evidence for ferroptosis—a form of regulated cell death driven by iron-dependent lipid peroxidation—as a key contributor to heart failure progression. The analysis shows ferroptosis is prevalent in the myocardium across diverse heart failure models, including those related to diabetic and obesity-related cardiomyopathy.

Ferroptosis: The Iron-Linked Heart Failure Nexus and Its Druggable Pathways A comprehensive review in Cardiovascular Research synthesizes evidence on ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, as a key contributor to heart failure progression. The analysis details how disordered iron handling, antioxidant failure, and mitochondrial stress converge in various cardiomyopathy models, leading to contractile dysfunction. Crucially, the review highlights that established cardiometabolic drugs with proven clinical efficacy—including Sodium–Glucose Cotransporter 2 (SGLT2) inhibitors, sacubitril/valsartan, and the non-steroidal mineralocorticoid receptor antagonist finerenone—demonstrate multi-layer rescue effects, restoring cardiac function and reversing adverse remodelling in preclinical studies.

Iron's Deadly Role in the Failing Heart A comprehensive review in *Cardiovascular Research* synthesizes evidence on ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, as a key contributor to heart failure. The analysis shows ferroptosis is abundant in the myocardium of animal models of diabetic cardiomyopathy, among others, where disordered iron handling and antioxidant failure converge to cause contractile dysfunction.

**Abstract:** Age-related cardiac dysfunction is significantly driven by the accumulation of senescent cardiac fibroblasts (CFs), contributing to fibrosis and impaired contractility. Current senescence clearance therapies often exhibit limited specificity and systemic toxicity. This research proposes a novel strategy utilizing targeted nanoparticles to selectively induce ferroptosis, a form of regulated cell death, within senescent CFs. This approach aims to achieve localized senescence elimination with minimized off-target effects, presenting a promising avenue for cardiac rejuvenation and age-associated heart failure treatment.

Genes & Immunity - Radiotherapy combined with anti-PD-1 immunotherapy promotes ferroptosis-driven control of hepatocellular carcinoma

The studies highlight reinforcing mechanisms and practical levers across minds, cells, and ecosystems.

Rizzollo et al. show that BDH2 participates in iron distribution between cellular compartments, which sets the threshold for the ferroptosis vulnerability of the melanoma cell phenotypes, ultimately a...

Rizzollo et al. show that BDH2 participates in iron distribution between cellular compartments, which sets the threshold for the ferroptosis vulnerability of the melanoma cell phenotypes, ultimately a...