Regulated cell death pathways in cardiomyopathy

Acta Pharmacologica Sinica, Journal Year: 2023, Volume and Issue: 44(8), P. 1521 - 1535

Published: March 13, 2023

Language: Английский

---

Non-coding RNA-mediated modulation of ferroptosis in cardiovascular diseases

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 164, P. 114993 - 114993

Published: June 9, 2023

Cardiovascular disease (CVD) is a major contributor to increasing morbidity and mortality worldwide seriously threatens human health life. Cardiomyocyte death considered the pathological basis of various CVDs, including myocardial infarction, heart failure, aortic dissection. Multiple mechanisms, such as ferroptosis, necrosis, apoptosis, contribute cardiomyocyte death. Among them, ferroptosis an iron-dependent form programmed cell that plays vital role in physiological processes, from development aging immunity CVD. The dysregulation has been shown be closely associated with CVD progression, yet its underlying mechanisms are still not fully understood. In recent years, growing amount evidence suggests non-coding RNAs (ncRNAs), particularly microRNAs, long RNAs, circular involved regulation thus affecting progression. Some ncRNAs also exhibit potential value biomarker and/or therapeutic target for patients this review, we systematically summarize findings on their We focus clinical applications diagnostic prognostic biomarkers well targets treatment. DATA AVAILABILITY: No new data were created or analyzed study. Data sharing applicable article.

Language: Английский

---

Potential Interactions When Prescribing SGLT2 Inhibitors and Intravenous Iron in Combination in Heart Failure

JACC Heart Failure, Journal Year: 2022, Volume and Issue: 11(1), P. 106 - 114

Published: Nov. 5, 2022

In patients with heart failure, sodium-glucose cotransporter 2 (SGLT2) inhibitors have been shown to decrease hepcidin and ferritin increase transferrin receptor protein, changes that are typically indicative of worsening absolute iron deficiency, as would be seen poor dietary intake or gastrointestinal bleeding, neither which is provoked by SGLT2 inhibitors. Therefore, alternative conceptual frameworks may explain the observed pattern in homeostasis proteins. According "cytosolic depletion hypothesis," effect related a decline cytosolic Fe2+ occurs after drug-induced erythropoietin-related use. Erythropoietin-mimetics (eg, darbepoietin) elicit this type iron-deficiency response, it accompanied erythropoietin resistance alleviated intravenous supplementation. contrast, according repletion represents direct action these drugs: 1) reverse inflammation-related increases ferritin, and, thus, alleviate functional blocks on utilization; 2) sirtuin-1 signaling, suppresses hepcidin, accelerates degradation up-regulates protein. Through either both mechanisms, suppression expected Fe2+, thus allowing an unattenuated erythrocytic response without need for The totality clinical evidence supports hypothesis" because full sustained erythrocytosis erythropoietin, even overtly iron-deficient absence therapy. emergence during inhibition does not reflect stores replenishment, but instead, potential alleviation state deficiency commonly chronic failure. Treatment unnecessary theoretically deleterious.

Language: Английский

---

How can sodium–glucose cotransporter 2 inhibitors stimulate erythrocytosis in patients who are iron‐deficient? Implications for understanding iron homeostasis in heart failure

European Journal of Heart Failure, Journal Year: 2022, Volume and Issue: 24(12), P. 2287 - 2296

Published: Nov. 15, 2022

Many patients with heart failure have an iron‐deficient state, which can limit erythropoiesis in erythroid precursors and ATP production cardiomyocytes. Yet, treatment sodium–glucose cotransporter 2 (SGLT2) inhibitors produces consistent increases haemoglobin haematocrit, even who are before treatment, this effect remains unattenuated throughout though SGLT2 further aggravate biomarkers of iron deficiency. Heart is often accompanied by systemic inflammation, activates hepcidin, thus impairing the duodenal absorption release from macrophages hepatocytes, leading to a decline circulating iron. Inflammation oxidative stress also promote synthesis ferritin suppress ferritinophagy, intracellular stores depletion bioreactive cytosolic Fe 2+ . By alleviating inflammation stress, down‐regulate upregulate transferrin receptor protein 1 reduce ferritin; net result increase levels available mitochondria, enabling heme (in precursors) cardiomyocytes). The finding that induce erythrocytosis without supplementation suggests abnormalities diagnostic tests mild‐to‐moderate likely be functional, rather than absolute, is, they related inflammation‐mediated trapping hepcidin ferritin, reversed inhibitors. An augment mitochondrial cardiomyocytes, retarding progression failure. These effects on metabolism (i) proteomics analyses placebo‐controlled trials, shown homeostasis represent most inhibitors; (ii) statistical mediation analyses, reported striking parallelism events.

Language: Английский

---

N6-methyladenosine writer METTL3 accelerates the sepsis-induced myocardial injury by regulating m6A-dependent ferroptosis

APOPTOSIS, Journal Year: 2023, Volume and Issue: 28(3-4), P. 514 - 524

Published: Jan. 16, 2023

Language: Английский

---

Mechanisms of ferroptosis regulating oxidative stress and energy metabolism in myocardial ischemia-reperfusion injury and a novel perspective of natural plant active ingredients for its treatment

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 165, P. 114706 - 114706

Published: July 1, 2023

Acute myocardial infarction remains the leading cause of death in humans. Timely restoration blood perfusion to ischemic myocardium most effective strategy treatment acute infarction, which can significantly reduce morbidity and mortality. However, after flow reperfusion, injury will aggravate induce apoptosis cardiomyocytes, a process called ischemia-reperfusion injury. Studies have shown that loss cardiomyocytes caused by oxidative stress, iron load, increased lipid peroxidation, inflammation mitochondrial dysfunction, etc., are involved In recent years, with in-depth research on pathology injury, people gradually realized there is new form cell pathological namely ferroptosis. A number studies found tissue patients changes closely related ferroptosis, such as metabolism disorder, reactive oxygen species free radicals. Natural plant products resveratrol, baicalin, cyanidin-3-O-glucoside, naringenin, astragaloside IV also exert therapeutic effects correcting imbalance these ferroptosis-related factors expression levels. Combining our previous studies, this review summarizes regulatory mechanism natural intervening ferroptosis order provide reference information for development targeted inhibitor drugs cardiovascular diseases.

Language: Английский

---

New Insights into the Role of Ferroptosis in Cardiovascular Diseases

Cells, Journal Year: 2023, Volume and Issue: 12(6), P. 867 - 867

Published: March 10, 2023

Cardiovascular diseases (CVDs) are the principal cause of disease burden and death worldwide. Ferroptosis is a new form regulated cell mainly characterized by altered iron metabolism, increased polyunsaturated fatty acid peroxidation reactive oxygen species, depletion glutathione inactivation peroxidase 4. Recently, series studies have indicated that ferroptosis involved in cardiac vascular cells has key impact on mechanisms leading to CVDs such as ischemic heart disease, ischemia/reperfusion injury, cardiomyopathies, failure. In this article, we reviewed molecular mechanism current understanding pathophysiological role some cardiomyopathies. Moreover, comprehension machinery governing cardiomyocytes may provide insights into preventive therapeutic strategies CVDs.

Language: Английский

---

Emerging regulatory mechanisms in cardiovascular disease: Ferroptosis

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 174, P. 116457 - 116457

Published: March 22, 2024

Ferroptosis, distinct from apoptosis, necrosis, autophagy, and other types of cell death, is a novel iron-dependent regulated death characterized by the accumulation lipid peroxides redox imbalance with morphological, biochemical, genetic features. Dysregulation iron homeostasis, disruption antioxidative stress pathways peroxidation are crucial in ferroptosis. Ferroptosis involved pathogenesis several cardiovascular diseases, including atherosclerosis, cardiomyopathy, myocardial infarction, ischemia-reperfusion injury, abdominal aortic aneurysm, dissection, heart failure. Therefore, comprehensive understanding mechanisms that regulate ferroptosis diseases will enhance prevention treatment these diseases. This review discusses latest findings on molecular its regulation application modulators role traditional Chinese medicines to provide identify new options.

Language: Английский

---

Acute exposure to tris(2,4-di-tert-butylphenyl)phosphate elicits cardiotoxicity in zebrafish (Danio rerio) larvae via inducing ferroptosis

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 471, P. 134389 - 134389

Published: April 23, 2024

Language: Английский

---

Targeting Lcn2 to Inhibit Myocardial Cell Ferroptosis is a Potential Therapy for Alleviating Septic Cardiomyopathy

Inflammation, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 3, 2025

Septic cardiomyopathy (SCM) represents a key feature of sepsis-associated cardiovascular failure, and ferroptosis is one the essential causes septic cardiac dysfunction. In this study, combined with omics analysis in vivo experiments, we verified damage on tissue mice mined target genes that can inhibit cardiomyocytes. Lipocalin-2 (Lcn2) was identified to be associated SCM progression via integrated transcriptomic proteomic analyses. Sepsis induced by cecal ligation perforation (CLP) mice. Ferroptosis dysfunction were detected pathological staining ELISA. However, after knockout Lcn2, cardiomyocyte significantly suppressed, inflammatory infiltrates reduced, reactive oxygen species (ROS) levels lowered, mitochondrial alleviated, function restored CLP summary, study found Lcn2 potential for inhibiting SCM. Targeting effectively inflammation, improve dysfunction, ferroptosis, alleviate

Language: Английский

---