Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation DOI Creative Commons
Z. Zhang, Jiawei Guo

Antioxidants, Journal Year: 2024, Volume and Issue: 14(1), P. 38 - 38

Published: Dec. 31, 2024

Oxidative stress plays a pivotal role in the pathogenesis and progression of cardiovascular diseases (CVDs). This review focuses on signaling pathways oxidative during development CVDs, delving into molecular regulatory networks underlying various disease stages, particularly apoptosis, inflammation, fibrosis, metabolic imbalance. By examining dual roles influences sex differences levels susceptibility, this study offers comprehensive understanding diseases. The integrates key findings from current research three ways. First, it outlines major CVDs associated with their respective pathways, emphasizing stress’s central pathology. Second, summarizes protective effects, mechanisms action, animal models antioxidants, offering insights future drug development. Third, discusses applications, advantages, limitations, potential targets gene therapy providing foundation for novel therapeutic strategies. These tables underscore systematic integrative nature while theoretical basis precision treatment CVDs. A contribution is differential effects across different stages addition to proposal innovative, multi-level intervention strategies, which open new avenues system.

Language: Английский

Inhibition of Sat1 alleviates myocardial ischemia-reperfusion injury through regulation of ferroptosis via MAPK/ERK pathway DOI Creative Commons
Zhou Liu,

Hongjin Chen,

Yingnan Song

et al.

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

Published: Nov. 13, 2024

Introduction Myocardial ischemia-reperfusion injury (MIRI) is a prevalent complication in patients with myocardial infarction. The pathological mechanism of MIRI remains elusive. Ferroptosis plays critical role MIRI. This study aimed to investigate the spermidine/spermine N1-acetyltransferase 1 (Sat1) by regulation ferroptosis. Methods Rats and H9C2 cells were used perform model. extent damage associated changes evaluated. Protein expression was detected western blot. Then we observed mitochondrial morphology measured cell viability damage. levels lipid peroxide glutathione measured, reactive oxygen species (ROS) quantified. Differentially expressed genes (DEGs) analyzed. Moreover, explore Sat1 MIRI, this utilized adeno-associated virus 9 lentiviral transduction modulate rats cells, respectively. transcription factor that regulates predicated. Luciferase reporter gene experiment conducted reveal potential sites Sox2 binding Sat1. Results revealed ferroptosis involved Through bioinformatic analysis, identified as significant which has been reported an inducer Our results showed significantly increased Next, inhibition alleviated suppressing vivo vitro , over-expression promoted via activation Furthermore, its interacting enriched several signaling pathways, including MAPK pathway. regulated through MAPK/ERK it found can suppress at transcriptional level. site TAACAAAGGAA. Conclusion In sum, demonstrated alleviate regulating pathway, negatively Sox2. These findings suggested may serve therapeutic target for treatment

Language: Английский

Citations

5
Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis DOI Creative Commons

Yuanbo Xu,

Piao Wang, Ting Hu

et al.

Current Issues in Molecular Biology, Journal Year: 2025, Volume and Issue: 47(1), P. 44 - 44

Published: Jan. 10, 2025

Mitochondrial homeostasis is crucial for maintaining cellular energy production and preventing oxidative stress, which essential overall function longevity. damage dysfunction often occur concomitantly in myocardial ischemia-reperfusion injury (MIRI). Notoginsenoside R1 (NGR1), a unique saponin from the traditional Chinese medicine Panax notoginseng, has been shown to alleviate MIRI previous studies, though its precise mechanism remains unclear. This study aimed elucidate mechanisms of NGR1 mitochondrial hypoxia/reoxygenation (H/R) H9c2 cells. The results showed that pretreatment effectively increased cell survival rates post-H/R, reduced lactate dehydrogenase (LDH) leakage, mitigated damage. Further investigation into mitochondria revealed alleviated structural damage, improved membrane permeability transition pore (mPTP) persistence, prevented potential (Δψm) depolarization. Additionally, enhanced ATP levels, activity respiratory chain complexes I-V after H/R, excessive reactive oxygen species (mitoROS) production, thereby protecting function. analysis indicated upregulated expression biogenesis-related proteins (PGC-1α, Nrf1, Nrf2) fusion (Opa1, Mfn1, Mfn2), while downregulating fission (Fis1, Drp1) reducing autophagy (mitophagy) as well mitophagy-related (Pink1, Parkin, BNIP3) post-H/R. Therefore, this can maintain by regulating mitophagy, fission-fusion dynamics, biogenesis, alleviating H/R cardiomyocytes.

Language: Английский

Citations

0
Hypoferremia reduces long-term risk of major adverse cardiovascular events after STEMI by averting the myocardial reactive iron storm DOI Creative Commons

Mayra Vera-Aviles,

S. Nashitha Kabir, Michalis Christodoulou

et al.

medRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 15, 2025

ABSTRACT Background and aims Iron deficiency (ID) is common in patients with acute STEMI. ID has previously been associated either adverse or favourable effects, depending on the definition of ID, sampling timepoint, outcome measures follow-up duration. This study systematically addresses impact long-term outcomes explores underlying mechanisms. Methods Patients STEMI (n=167) were followed for 4.5 years major cardiovascular events (MACE), including new HF diagnosis, recurrent MI cardiac death. markers sampled at presentation later timepoints. Myocardial injury was assessed by CMR 2 days 6 months. Mechanisms clinical findings evaluated a mouse model MI. Results any definition, presentation. Hypoferremia (Tsat<20% iron<13uM) but not hypoferritinemia (ferritin<100ug/L) predicted lower risk MACE. troponin, myocardial T1, LVESV LVEDV days, salvage status from hours after no longer In mice, rapidly triggered reactive iron storm, early LV remodelling, eventually HF. These effects averted restriction. Conclusions reveals that hypoferremia exerts both nonetheless translate into better outcomes. research reconciles previous seemingly conflicting reports. It also highlights potential stepwise approach chelation to reduce injury, supplementation promote salvage.

Language: Английский

Citations

0
Regulation of Iron Metabolism in Ferroptosis: from Mechanism Research to Clinical Translation DOI Creative Commons
Xin Zhang, Xiang Yang, Qingyan Wang

et al.

Journal of Pharmaceutical Analysis, Journal Year: 2025, Volume and Issue: unknown, P. 101304 - 101304

Published: April 1, 2025

Language: Английский

Citations

0
Deciphering Oxidative Stress in Cardiovascular Disease Progression: A Blueprint for Mechanistic Understanding and Therapeutic Innovation DOI Creative Commons
Z. Zhang, Jiawei Guo

Antioxidants, Journal Year: 2024, Volume and Issue: 14(1), P. 38 - 38

Published: Dec. 31, 2024

Oxidative stress plays a pivotal role in the pathogenesis and progression of cardiovascular diseases (CVDs). This review focuses on signaling pathways oxidative during development CVDs, delving into molecular regulatory networks underlying various disease stages, particularly apoptosis, inflammation, fibrosis, metabolic imbalance. By examining dual roles influences sex differences levels susceptibility, this study offers comprehensive understanding diseases. The integrates key findings from current research three ways. First, it outlines major CVDs associated with their respective pathways, emphasizing stress’s central pathology. Second, summarizes protective effects, mechanisms action, animal models antioxidants, offering insights future drug development. Third, discusses applications, advantages, limitations, potential targets gene therapy providing foundation for novel therapeutic strategies. These tables underscore systematic integrative nature while theoretical basis precision treatment CVDs. A contribution is differential effects across different stages addition to proposal innovative, multi-level intervention strategies, which open new avenues system.

Language: Английский

Citations

2