Research advances on molecular mechanism and natural product therapy of iron metabolism in heart failure DOI Creative Commons
Tianqing Zhang,

Li Luo,

Qi He

et al.

European journal of medical research, Journal Year: 2024, Volume and Issue: 29(1)

Published: April 24, 2024

Abstract The progression of heart failure (HF) is complex and involves multiple regulatory pathways. Iron ions play a crucial supportive role as cofactor for important proteins such hemoglobin, myoglobin, oxidative respiratory chain, DNA synthetase, in the myocardial energy metabolism process. In recent years, numerous studies have shown that HF associated with iron dysmetabolism, deficiencies overload can both lead to development various myocarditis diseases, which ultimately progress HF. toxicity may be key targets diagnosis, treatment, prevention Some chelators (such desferrioxamine), antioxidants ascorbate), Fer-1, molecules regulate levels lactoferrin) been effective treating protecting myocardium studies. Additionally, certain natural compounds significant by mediating imbalance iron-related signaling pathways expression levels. Therefore, this review not only summarizes basic processes body mechanisms they HF, aim providing new clues considerations treatment but also on chemical components involve ferroptosis its pathology, well naturally occurring products reference information inhibitors future.

Language: Английский

The mechanism of ferroptosis and its related diseases DOI Creative Commons
Shijian Feng, Dan Tang, Yichang Wang

et al.

Molecular Biomedicine, Journal Year: 2023, Volume and Issue: 4(1)

Published: Oct. 16, 2023

Abstract Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation lipid peroxides, provides novel avenue for delving into intersection metabolism, oxidative stress, and disease pathology. We have witnessed mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, traumatic tissue injuries. By unraveling intricate underpinnings molecular machinery, contributors, signaling conduits, regulatory networks governing researchers aim bridge gap between intricacies this unique mode multifaceted implications health disease. In light rapidly advancing landscape ferroptosis research, we present comprehensive review aiming at extensive in origins progress human diseases. This concludes careful analysis potential treatment approaches carefully designed either inhibit or promote ferroptosis. Additionally, succinctly summarized therapeutic targets compounds that hold promise targeting within various facet underscores burgeoning possibilities manipulating as strategy. summary, enriched insights both investigators practitioners, while fostering an elevated comprehension latent translational utilities. revealing basic processes investigating possibilities, crucial resource scientists medical aiding deep understanding effects situations.

Language: Английский

Citations

64
Idebenone alleviates doxorubicin-induced cardiotoxicity by stabilizing FSP1 to inhibit ferroptosis DOI Creative Commons

Hong-liang Qiu,

Sihui Huang, Yuting Liu

et al.

Acta Pharmaceutica Sinica B, Journal Year: 2024, Volume and Issue: 14(6), P. 2581 - 2597

Published: March 11, 2024

Doxorubicin (DOX)-mediated cardiotoxicity can exacerbate mortality in oncology patients, but related pharmacotherapeutic measures are relatively limited. Ferroptosis was recently identified as a major mechanism of DOX-induced cardiotoxicity. Idebenone, novel ferroptosis inhibitor, is well-described clinical drug widely used. However, its role and pathological still unclear. In this study, we demonstrated the effects idebenone on elucidated underlying mechanism. A single intraperitoneal injection DOX (15 mg/kg) administrated to establish The results showed that significantly attenuated cardiac dysfunction due ability regulate acute Fe2+ ROS overload, which resulted ferroptosis. CESTA BLI further revealed idebenone's anti-ferroptosis effect mediated by FSP1. Interestingly, increased FSP1 protein levels did not affect Fsp1 mRNA presence DOX. Idebenone could form stable hydrogen bonds with at K355, may influence association ubiquitin. confirmed stabilized inhibiting ubiquitination degradation. conclusion, study demonstrates via regulation FSP1, making it potential for patients receiving treatment.

Language: Английский

Citations

20
Ferroptosis in cardiovascular disease DOI Open Access
Guoqing Liu, Xiaoyong Xie, Wang Liao

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 170, P. 116057 - 116057

Published: Dec. 29, 2023

In the 21st century, cardiovascular disease (CVD) has become one of leading causes death worldwide. The prevention and treatment CVD remain pressing scientific issues. Several recent studies have suggested that ferroptosis may play a key role in CVD. Most conducted thus far on supported link. Ferroptosis mediated by different signaling metabolic pathways can lead to ischemic heart disease, myocarditis, failure, ischemia-reperfusion injury, cardiomyopathy. Still, specific mechanism CVD, particular organ areas affected, stage involved need be further studied. Therefore, understanding mechanisms regulating improve management. Throughout this review, we summarized its effect pathogenesis We also predicted discussed future research directions, aiming provide new ideas strategies for preventing treating

Language: Английский

Citations

24
Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury DOI Open Access
V. V. Ryabov, Л. Н. Маслов,

Evgeniy V. Vyshlov

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(2), P. 897 - 897

Published: Jan. 11, 2024

The hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) is about 6% and has not decreased recent years. leading cause of death these ischemia/reperfusion (I/R) cardiac injury. It quite obvious that there an urgent need to create new drugs for the treatment STEMI based on knowledge pathogenesis I/R injury, particular, molecular mechanism ferroptosis. In this study, it was demonstrated ferroptosis involved development antitumor drug-induced cardiomyopathy, diabetic septic inflammation. There indirect evidence participates stress-induced activation AMPK, PKC, ERK1/2, PI3K, Akt prevents inhibition HO-1 alleviates roles GSK-3β NOS regulation require further study. stimulation Nrf2, STAT3 TLR4 NF-κB promotes cardiomyocytes. MiR-450b-5p miR-210-3p can increase tolerance cardiomyocytes hypoxia/reoxygenation through Circ_0091761 RNA, miR-214-3p, miR-199a-5p, miR-208a/b, miR-375-3p, miR-26b-5p miR-15a-5p aggravate

Language: Английский

Citations

12
Mitochondrial Dysfunction in Cardiac Diseases and Therapeutic Strategies DOI Creative Commons
Yafei Huang, Bingying Zhou

Biomedicines, Journal Year: 2023, Volume and Issue: 11(5), P. 1500 - 1500

Published: May 22, 2023

Mitochondria are the main site of intracellular synthesis ATP, which provides energy for various physiological activities cell. Cardiomyocytes have a high density mitochondria and mitochondrial damage is present in variety cardiovascular diseases. In this paper, we describe cardiomyopathy, congenital heart disease, coronary myocardial ischemia-reperfusion injury, failure, drug-induced cardiotoxicity, context key roles cardiac development homeostasis. Finally, discuss current therapeutic strategies aimed at alleviating impairment-related dysfunction, including pharmacological strategies, gene therapy, replacement transplantation. It hoped that will provide new ideas treatment

Language: Английский

Citations

17
The protective role of ginsenoside Rg3 in heart diseases and mental disorders DOI Creative Commons
Lili Shi, Jinlan Luo,

Xiupan Wei

et al.

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

Published: Feb. 26, 2024

Ginsenoside Rg3, a compound derived from

Language: Английский

Citations

8
Hypoxia-associated autophagy flux dysregulation in human cancers DOI
Jiding Fu,

Jie Lin,

Zili Dai

et al.

Cancer Letters, Journal Year: 2024, Volume and Issue: 590, P. 216823 - 216823

Published: March 21, 2024

Language: Английский

Citations

8
Differential expression profiles of plasma exosomal microRNAs in dilated cardiomyopathy with chronic heart failure DOI Creative Commons
Li Zhang, Ge Zhang,

Yongzheng Lu

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2023, Volume and Issue: 27(14), P. 1988 - 2003

Published: May 27, 2023

As one of the most prevalent heritable cardiovascular diseases, dilated cardiomyopathy (DCM) induces cardiac insufficiency and dysfunction. Although genetic mutation has been identified causes DCM, usage biomarkers such as RNAs for DCM early diagnosis is still being overlooked. In addition, alternation could reflect progression an indicator prognosis patients. Therefore, it beneficial to develop based diagnostic tool DCM. are often unstable within circulatory system, leading infeasibility clinical application. Recently discovered exosomal miRNAs have stability that then need purpose. Hence, fully understanding miRNA patients vital translation. this study, we employed next generation sequencing on plasma comprehensively characterize expression in exosomes from exhibiting chronic heart failure (CHF) compared healthy individuals. A complex landscape differential target genes with CHF were identified. More importantly, 92 differentially expressed undergoing correlated several enriched pathways, including oxytocin signalling pathway, circadian entrainment, hippo pathway-multiple species, ras pathway morphine addiction. This study reveals profiles CHF, further reveal their potential roles pathogenesis it, presenting a new direction management CHF.

Language: Английский

Citations

16
Atherosclerotic plaque vulnerability quantification system for clinical and biological interpretability DOI Creative Commons
Ge Zhang, Xiaolin Cui, Zhenpeng Qin

et al.

iScience, Journal Year: 2023, Volume and Issue: 26(9), P. 107587 - 107587

Published: Aug. 9, 2023

Acute myocardial infarction dominates coronary artery disease mortality. Identifying bio-signatures for plaque destabilization and rupture is important preventing the transition from stability to instability occurrence of thrombosis events. This computational systems biology study enrolled 2,235 samples 22 independent bulks cohorts 14 two single-cell cohorts. A machine-learning integrative program containing nine learners was developed generate a warning classifier linked atherosclerotic vulnerability signature (APVS). The displays reliable performance robustness distinguishing ST-elevation chronic syndrome at presentation, revealed higher accuracy 33 pathogenic biomarkers. We also an APVS-based quantification system (APVSLevel) comprehensively quantifying vulnerability, empowering early-warning capabilities, accurate assessment atherosclerosis severity. It unraveled multidimensional dysregulated mechanisms high resolution. provides potential tool macro-level differential diagnosis evaluation subtle genetic pathological changes in atherosclerosis.

Language: Английский

Citations

11
An assessment system for clinical and biological interpretability in ulcerative colitis DOI Creative Commons

Shiqian Zhang,

Ge Zhang, Wenxiu Wang

et al.

Aging, Journal Year: 2024, Volume and Issue: 16(4), P. 3856 - 3879

Published: Feb. 16, 2024

Aging | doi:10.18632/aging.205564. Shiqian Zhang, Ge Wenxiu Wang, Song-Bin Guo, Pengpeng Fuqi Quanbo Zhou, Zhaokai Yujia Haifeng Sun, Wenming Cui, Shuaixi Yang, Weitang Yuan

Citations

4