Ferroptosis in diabetic cardiomyopathy: from its mechanisms to therapeutic strategies DOI Creative Commons

Meimei Tian,

Xinli Huang, Min Li

et al.

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 11, 2024

Diabetic cardiomyopathy (DCM) is defined as structural and functional cardiac abnormalities in diabetes, cardiomyocyte death the terminal event of DCM. Ferroptosis iron-dependent oxidative cell death. Evidence has indicated that iron overload ferroptosis play important roles pathogenesis Mitochondria, an organelle homeostasis ROS production, a crucial role diabetes. Studies have shown some anti-diabetic medicines, plant extracts, inhibitors might improve DCM by alleviating ferroptosis. In this review, we systematically reviewed evidence Anti-ferroptosis be promising therapeutic strategy for treatment

Language: Английский

Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects DOI Creative Commons

Qin Ru,

Yusheng Li,

Lin Chen

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: Oct. 14, 2024

Iron, an essential mineral in the body, is involved numerous physiological processes, making maintenance of iron homeostasis crucial for overall health. Both overload and deficiency can cause various disorders human diseases. Ferroptosis, a form cell death dependent on iron, characterized by extensive peroxidation lipids. Unlike other kinds classical unprogrammed death, ferroptosis primarily linked to disruptions metabolism, lipid peroxidation, antioxidant system imbalance. Ferroptosis regulated through transcription, translation, post-translational modifications, which affect cellular sensitivity ferroptosis. Over past decade or so, diseases have been as part their etiology, including cancers, metabolic disorders, autoimmune diseases, central nervous cardiovascular musculoskeletal Ferroptosis-related proteins become attractive targets many major that are currently incurable, some regulators shown therapeutic effects clinical trials although further validation potential needed. Therefore, in-depth analysis its molecular mechanisms may offer additional strategies prevention treatment. In this review, we discuss significance contribution etiology development along with evidence supporting targeting approach. Importantly, evaluate recent promising interventions, providing guidance future targeted treatment therapies against

Language: Английский

Citations

64
Molecular Mechanisms Underlying Heart Failure and Their Therapeutic Potential DOI Creative Commons
Oveena Fonseka, Sanskruti Ravindra Gare, Xinyi Chen

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(5), P. 324 - 324

Published: Feb. 20, 2025

Heart failure (HF) is a prominent fatal cardiovascular disorder afflicting 3.4% of the adult population despite advancement treatment options. Therefore, better understanding pathogenesis HF essential for exploring novel therapeutic strategies. Hypertrophy and fibrosis are significant characteristics pathological cardiac remodeling, contributing to HF. The mechanisms involved in development remodeling consequent multifactorial, this review, key underlying discussed. These have been divided into following categories thusly: (i) mitochondrial dysfunction, including defective dynamics, energy production, oxidative stress; (ii) lipotoxicity; (iii) maladaptive endoplasmic reticulum (ER) (iv) impaired autophagy; (v) inflammatory responses; (vi) programmed cell death, apoptosis, pyroptosis, ferroptosis; (vii) endothelial dysfunction; (viii) contractility. Preclinical data suggest that there merit targeting identified pathways; however, their clinical implications outcomes regarding treating need further investigation future. Herein, we introduce molecular pivotal onset progression HF, as well compounds related potential preventing or rescuing This, therefore, offers an avenue design discovery therapies

Language: Английский

Citations

2
Shen-fu Injection Modulates HIF- 1α/BNIP3-Mediated Mitophagy to Alleviate Myocardial Ischemia–Reperfusion Injury DOI
Zhian Chen, Tianying Liu, Li Xiong

et al.

Cardiovascular Toxicology, Journal Year: 2025, Volume and Issue: unknown

Published: April 17, 2025

Language: Английский

Citations

1
Calycosin alleviates ferroptosis and attenuates doxorubicin-induced myocardial injury via the Nrf2/SLC7A11/GPX4 signaling pathway DOI Creative Commons

Quancheng Han,

Jingle Shi,

Yiding Yu

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 12, 2024

Background Heart failure is primarily characterized by damage to the structure and function of heart. Ferroptosis represents a form programmed cell death, studies indicate that it constitutes one primary mechanisms underlying cardiomyocyte death in heart failure. Calycosin, natural compound derived from astragalus, exhibits various pharmacological properties, including anti-ferroptosis, antioxidant effects, cardiovascular protection. Nonetheless, specific role Calycosin treatment ferroptosis remains poorly understood. Objective This study aims elucidate regulatory effect on its influence through vivo vitro experiments. Methods A rat model was induced using doxorubicin, cardiac evaluated ultrasound examination NT-Pro BNP detection. Myocardial injury assessed H&E staining Masson staining. The extent mitochondrial transmission electron microscopy. Concurrently, level analyzed measuring markers, MDA, ferrous ions, GSH/GSSG ratio, GPX4 activity. Subsequently, molecular mechanism which exerts therapeutic effects investigated immunofluorescence Western blotting. Finally, H9c2 cardiomyocytes were treated with doxorubicin simulate myocardial injury, mediates further verified Nrf2 gene silencing. Results significantly improves rats, reduces serum levels, alleviates damage. Additionally, decreases levels tissue, as confirmed microscopy assessment GSH, At level, activating Nrf2/SLC7A11/GPX4 signaling pathway, evidenced upregulation Nrf2, SLC7A11, GPX4, GSS, GCL protein expression. process substantially enhances capacity tissue effectively suppresses cells. results obtained both experiments are consistent. Notably, when silenced, protective myocardium markedly diminished. Conclusion treats doxorubicin-induced likely closely associated activation pathway inhibition Consequently, promising against cardiotoxicity, warrants investigation.

Language: Английский

Citations

4
Key Mechanisms of Oxidative Stress-Induced Ferroptosis in Heart Failure with Preserved Ejection Fraction and Potential Therapeutic Approaches DOI Creative Commons

Junling Lin,

Bingtao Li,

Xueqi Guo

et al.

Reviews in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 26(3)

Published: March 25, 2025

The prevalence of heart failure with preserved ejection fraction (HFpEF) is increasing annually, particularly among patients metabolic disorders such as hypertension and diabetes. However, there currently no treatment capable altering the natural course HFpEF. Recently, interplay between oxidative stress ferroptosis in cardiovascular diseases has drawn extensive attention; however, minimal research been published on mechanisms This paper reviews relevant through which induced promotes during development review also explores more efficacious approaches for HFpEF by inhibiting ferroptosis, thereby offering a theoretical foundation verifying feasibility these methods further research. As tumor-targeted therapy progresses, survival period tumor prolonged, events have gradually emerged one most crucial causes death patients. Hence, vascular endothelial growth factor (VEGF) pathway become major target treatment, significantly enhancing patient survival. Nevertheless, secondary complications events, myocardial injury subsequent failure, severely impacted quality life. Therefore we explored potential mechanism novel targeted anti-cancer drugs induce via ferroptosis. Additionally, reviewed specific modes action preventing treating without influencing their therapeutic effect.

Language: Английский

Citations

0
Advances in Mechanisms of Ferroptosis in Cardiovascular Disease DOI

婷 李

Advances in Clinical Medicine, Journal Year: 2025, Volume and Issue: 15(04), P. 1433 - 1440

Published: Jan. 1, 2025

Language: Английский

Citations

0
Mechanistic role of environmental toxicants in inducing cellular ferroptosis and its associated diseases DOI
Hong Chen,

Bingchun Liu,

Peixin Xu

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2025, Volume and Issue: 298, P. 118269 - 118269

Published: May 10, 2025

Language: Английский

Citations

0
Ferroptosis in diabetic cardiomyopathy: from its mechanisms to therapeutic strategies DOI Creative Commons

Meimei Tian,

Xinli Huang, Min Li

et al.

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 11, 2024

Diabetic cardiomyopathy (DCM) is defined as structural and functional cardiac abnormalities in diabetes, cardiomyocyte death the terminal event of DCM. Ferroptosis iron-dependent oxidative cell death. Evidence has indicated that iron overload ferroptosis play important roles pathogenesis Mitochondria, an organelle homeostasis ROS production, a crucial role diabetes. Studies have shown some anti-diabetic medicines, plant extracts, inhibitors might improve DCM by alleviating ferroptosis. In this review, we systematically reviewed evidence Anti-ferroptosis be promising therapeutic strategy for treatment

Language: Английский

Citations

2