TTK Inhibition Alleviates Postinjury Neointimal Formation and Atherosclerosis DOI Creative Commons

Jiehong Wu,

Yu‐Xiao Liu,

Jiabin Zong

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 24, 2024

Atherosclerosis and its associated cardio-cerebrovascular complications remain the leading causes of mortality worldwide. Current lipid-lowering therapies reduce only approximately one-third cardiovascular risk. Furthermore, vascular restenosis thrombotic events following surgical interventions for severe stenosis significantly contribute to treatment failure. This highlights urgent need novel therapeutic targets manage atherosclerosis prevent thrombosis after injury. study identifies TTK protein kinase (TTK) as a key regulator smooth muscle cell (VSMC) phenotypic switching in context postinjury neointimal formation atherosclerosis. Mechanistically, upregulation VSMCs phosphorylates p120-catenin, β-catenin nuclear accumulation dissociation myocardin (MYOCD)/serum response factor (SRF) complex. Deletion specifically reduces injury models attenuates atherosclerotic lesions ApoE

Language: Английский

The Multifaceted Role of Endothelial Sirt1 in Vascular Aging: An Update DOI Creative Commons
Roberto Campagna, Laura Mazzanti, Veronica Pompei

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(17), P. 1469 - 1469

Published: Sept. 1, 2024

NAD+-dependent deacetylase sirtuin-1 (Sirt1) belongs to the sirtuins family, known be longevity regulators, and exerts a key role in prevention of vascular aging. By aging, expression levels Sirt1 decline with severe impact on function, such as rise endothelial dysfunction, which turn promotes development cardiovascular diseases. In this context, activity preventing senescence is particularly important. Given counteracting senescence, great efforts have been made deepen knowledge about intricate cross-talks interactions other molecules, order set up possible strategies boost prevent or treat The aim review provide proper background regulation function endothelium discuss recent advances regarding therapeutic targeting counteract

Language: Английский

Citations

11
UGP2, a novel target gene of TP53, inhibits endothelial cells apoptosis and atherosclerosis DOI
Ruyi Zhang, Xin He,

Juan-Jiang Chen

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: unknown, P. 123393 - 123393

Published: Jan. 1, 2025

Language: Английский

Citations

1
TRIM21 Promotes Endothelial Cell Activation via Accelerating SOCS3 Ubiquitination Degradation in Atherosclerosis DOI

Zhenxuan Hao,

Yihuan Wang,

Linlin Chen

et al.

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

Published: Feb. 8, 2025

Language: Английский

Citations

1
The Interplay Between Endoplasmic Reticulum Stress and Ferroptosis in Neurological Diseases DOI

Tianyu Zhai,

Bingbing Wang,

Caizhen Shi

et al.

Neurochemical Research, Journal Year: 2025, Volume and Issue: 50(2)

Published: Feb. 10, 2025

Language: Английский

Citations

1
Lactiplantibacillus plantarum JS19-adjunctly fermented goat milk alleviates D-galactose-induced aging by modulating oxidative stress and intestinal microbiota in mice DOI Creative Commons
Chao He,

Yazhou Mao,

Lusha Wei

et al.

Journal of Dairy Science, Journal Year: 2024, Volume and Issue: 107(10), P. 7564 - 7577

Published: May 31, 2024

Oxidative stress is a crucial factor in the age-related decline physiological, genomic, metabolic, and immunological functions. We screened Lactiplantibacillus plantarum JS19, which has been shown to possess therapeutic properties mice with ulcerative colitis. In this study, L. JS19 used as adjunct starter culture fermented goat milk (LAF) was employed alleviate d-galactose-induced aging regulate intestinal flora an mouse model. The oral administration of LAF effectively improved health spleen kidney mice, while mitigating hepatocyte oxidative damage induced by d-galactose. Additionally, alleviated dysbiosis reducing abundance harmful bacteria Desulfovibrio Helicobacter, greatly promoting growth beneficial Rikenellaceae_RC9_gut_group Eubacterium. Biomarker 5-hydroxyindole-3-acetic acid found be positively linked those bacteria, whereas bio-active metabolites were strongly correlated genus. These observations suggest that possesses capability mitigate effects model through regulation stress, gut microbiota composition, levels fecal metabolites. Consequently, these findings shed light on potential functional food antiaging properties.

Language: Английский

Citations

4
Angiotensin II: Role in oxidative stress, endothelial dysfunction, and diseases DOI
Amir Ajoolabady, Domenico Praticò, Jun Ren

et al.

Molecular and Cellular Endocrinology, Journal Year: 2024, Volume and Issue: 592, P. 112309 - 112309

Published: June 10, 2024

Language: Английский

Citations

4
SET7 lysine methyltransferase mediates the up-regulation of NADPH oxidase expression, oxidative stress, and NLRP3 inflammasome priming in atherosclerosis DOI Creative Commons
Simona‐Adriana Manea,

Mihaela-Loredana Vlad,

Alexandra-Gela Lazar

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 17, 2025

Dysregulation of histone methylation-based epigenetic mechanisms leads to either transient or long-lasting transcriptomic alterations in vascular and immune cells with important consequences on atherosclerotic plaque development stability. We hypothesized that the enzyme SET7 lysine methyltransferase contributes up-regulation NADPH oxidase (Nox) NLRP3 inflammasome expression atherosclerosis. To test this hypothesis, we examined human non-atherosclerotic tissue samples, apolipoprotein E-deficient (ApoE-/-) mice, macrophages (Mac) employing real-time PCR, Western blot, immunofluorescence microscopy, histological techniques. Male ApoE-/- mice established atherosclerosis were randomized receive concomitant high-fat diet, 5 mg/kg (R)-PFI-2, a selective pharmacological inhibitor, its vehicle, every other day for 4 weeks. The results revealed mRNA protein, H3K4me1 levels significantly elevated carotid lesions, aorta cultured pro-inflammatory Mac. In blockade catalytic activity specific reduced development, decreased aortic protein Nox subunits, mitigated formation NT-/4HNE-protein adducts, attenuated gene expression, pro-caspase-1 pro-IL18 cleavage. polarized M1-Mac, SET7-oriented intervention transcriptional NLRP3, caspase-1, IL1β, IL18, secretion IL1β TNFα. Transient overexpression endothelial enhanced Nox1, Nox2, Nox4, Nox5, p22phox. novel show regulates leading reactive oxygen species cytokines release data recommend as promising target interventions supportive therapeutic strategy cardiovascular diseases.

Language: Английский

Citations

0
The Hormetic Adaptative Capacity and Resilience to Oxidative Stress Is Strengthened by Exposome Enrichment with Air Cold Atmospheric Plasma: A Metabolome Targeted Follow-Up Approach DOI Creative Commons
Lucía González-Llorente, Miguel Ángel Andrés Gasco, Miguel Aranda

et al.

Biomedicines, Journal Year: 2025, Volume and Issue: 13(4), P. 949 - 949

Published: April 12, 2025

Background/Objectives: The exposome, encompassing all environmental influences on health, plays a pivotal role in oxidative stress-related diseases. Negative air ions (NAIs), generated via cold atmospheric plasma (CAP), have been proposed as potential modulators of resilience. This study aims to investigate the metabolic adaptations induced by prolonged exposure an NAI-enriched environment mice, focusing its effects stress markers and energy metabolism liver blood. Methods: Twenty male C57BL/6J mice were divided into four groups: two experimental groups exposed Air Cold Atmospheric Plasma–Nanoparticle Removal (aCAP-NR) device for either 18 days (short-term, ST) or 28 (long-term, LT), control without exposure. Targeted metabolomics was performed whole blood using ultra-high-performance liquid chromatography–mass spectrometry (UHPLC-MS). Statistical pathway analyses conducted assess alterations. Results: Metabolic profiling revealed significant shifts pathways, including enhanced glutathione metabolism, reduced lipid peroxidation, modulation purine metabolism. Short-term led increased mitochondrial efficiency homeostasis, while long-term adaptive reprogramming, with higher inosine levels suggesting antioxidant anti-inflammatory responses. No adverse systemic hepatic health observed. Conclusions: NAI aCAP-NR elicits hormetic response, enhancing resilience stress. These findings suggest that controlled enrichment NAIs may serve novel non-invasive strategy mitigating damage improving adaptative capacity stress, warranting further translational research.

Language: Английский

Citations

0
TTK Inhibition Alleviates Postinjury Neointimal Formation and Atherosclerosis DOI Creative Commons

Jiehong Wu,

Yu‐Xiao Liu,

Jiabin Zong

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 24, 2024

Atherosclerosis and its associated cardio-cerebrovascular complications remain the leading causes of mortality worldwide. Current lipid-lowering therapies reduce only approximately one-third cardiovascular risk. Furthermore, vascular restenosis thrombotic events following surgical interventions for severe stenosis significantly contribute to treatment failure. This highlights urgent need novel therapeutic targets manage atherosclerosis prevent thrombosis after injury. study identifies TTK protein kinase (TTK) as a key regulator smooth muscle cell (VSMC) phenotypic switching in context postinjury neointimal formation atherosclerosis. Mechanistically, upregulation VSMCs phosphorylates p120-catenin, β-catenin nuclear accumulation dissociation myocardin (MYOCD)/serum response factor (SRF) complex. Deletion specifically reduces injury models attenuates atherosclerotic lesions ApoE

Language: Английский

Citations

1