Mechanosensor Piezo1-Mediated Smooth Muscular Cell Pyroptosis Contributes to Vascular Calcification DOI
Jun Tao,

Daiting You,

Zejiang Feng

et al.

Published: Jan. 1, 2024

Language: Английский

Trimethylamine N-oxide induces cardiac diastolic dysfunction by down-regulating Piezo1 in mice with heart failure with preserved ejection fraction DOI
Qianwang Chen, Huaxing Zhang, Yuhong Chen

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: 369, P. 123554 - 123554

Published: March 11, 2025

Language: Английский

Citations

0

REDOX Imbalance and Oxidative Stress in the Intervertebral Disc: The Effect of Mechanical Stress and Cigarette Smoking on ER Stress and Mitochondrial Dysfunction DOI Creative Commons
Hui Li, Joshua B. Kelley,

Y.G. Ye

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(8), P. 613 - 613

Published: April 19, 2025

Low back pain is a widespread condition that significantly impacts quality of life, with intervertebral disc degeneration (IDD) being major contributing factor. However, the underlying mechanisms IDD remain poorly understood, necessitating further investigation. Environmental risk factors, such as mechanical stress and cigarette smoke, elevate reactive oxygen species levels from both endogenous exogenous sources, leading to redox imbalance oxidative stress. The endoplasmic reticulum (ER) mitochondria, two key organelles responsible for protein folding energy production, respectively, are particularly vulnerable Under conditions, ER mitochondrial dysfunction occur, resulting in unfolded response activation, impaired biosynthetic processes, disruptions tricarboxylic acid cycle electron transport chain, ultimately compromising metabolism. Prolonged excessive can trigger apoptosis through ER–mitochondrial crosstalk. Given unique microenvironment (IVD)—characterized by hypoxia, glucose starvation, region-specific cellular heterogeneity—the differential effects environmental stressors on distinct IVD cell populations require This review explores potential which factors alter activities, progression, discusses future therapeutic strategies aimed at mitigating degeneration.

Language: Английский

Citations

0

SETD7 drives diabetic endothelial dysfunction through FBXO45-mediated GPX4 ubiquitylation DOI Creative Commons
Wen Zhong,

Ruoxue Chen,

Jialin Zhao

et al.

Cardiovascular Diabetology, Journal Year: 2025, Volume and Issue: 24(1)

Published: April 24, 2025

Vasculopathy is the most prevalent complication of diabetes. Endothelial damage, a primary contributor to hyperglycemic vascular complications, impacts macro- and micro-vasculatures, causing functional impairment multiple organs. SETD7 was initially identified as transcriptional activator based on its ability methylate histone 3 lysine 4. However, function in context diabetic endothelial dysfunction remains poorly understood. This study aims elucidate involvement underlying mechanisms dysfunction. knockout mice were generated investigate effects Streptozotocin (STZ)-induced hyperglycemia injury. Endothelial-specific interruption adeno-associated virus (AAV) system utilized injury BKS-DB(Lepr) KO/KO (db/db) mice. In vitro manipulation activation or knockdown conducted assess regulation lipid peroxidation, oxidative stress, cell rat aortic cells (RAECs) under high glucose conditions. Our revealed that deficiency partially restored damaged attenuated inflammatory response caused by both STZ-induced db/db Moreover, aggravated stress resulted profound through Glutathione Peroxidase 4 (GPX4)-mediated peroxidation RAECs. Mechanistically, reduced p53 mono-methylation blocked FBXO45 transcription, thereby inhibiting protein degradation GPX4 subsequent well stress. summary, our demonstrates SETD7-p53-FBXO45-GPX4 involved glucose-induced exacerbated dysfunction, which offering great significance for mitigating hyperglycemia-induced damage.

Language: Английский

Citations

0

Mechanosensitive apoptosis in Alzheimer’s disease DOI Open Access

G.V. Sapozhnikov,

Rajesh Ranganathan, Shoutang Wang

et al.

Ageing and Neurodegenerative Diseases, Journal Year: 2025, Volume and Issue: 5(2)

Published: April 28, 2025

The incidence of neurodegenerative diseases is increasing exponentially, with Alzheimer’s disease (AD) being a notorious example. AD progressive, aging-related, multifactorial disease, and no uniform theory exists regarding its etiology. One hypothesis implicates defects in the organism’s mechanosensing mechanotransduction mechanisms. deleterious effects mechanical stress neurodegeneration have been proven through multiple studies observations, but pathways linking inputs to progression remain unclear. It has proposed that nervous tissue primarily responds sources astrocytes microglia, activation Piezo1 TRPV4 ion channels. An area current research examining might be involved elevated oxidative dysregulated apoptotic pathways. We summarized understanding related AD. Our review indicated relationship between crucial Hippo pathway (MST1 humans) KCNN4 worth following up future studies. noted G3BP1 G3BP2 FlnA-mediated are linked ceramide production, along their interaction granules - key element for onset apoptosis, which assembled, among others, response stress. This sheds light on how input disrupts what implications also identifies potential targets focus.

Language: Английский

Citations

0

ITGA5 drives angiogenesis in diabetic retinopathy via TAK-1/NF-kB activation DOI

Feifei Kan,

Di Wang, Sijia Li

et al.

Human Cell, Journal Year: 2025, Volume and Issue: 38(4)

Published: May 23, 2025

Language: Английский

Citations

0

Oxidative and Nitrous Stress Underlies Vascular Malfunction Induced by Ionizing Radiation and Diabetes DOI
Anatoly Soloviev, Vadym Sydorenko

Cardiovascular Toxicology, Journal Year: 2024, Volume and Issue: 24(8), P. 776 - 788

Published: June 25, 2024

Language: Английский

Citations

3

Immune and Metabolic Mechanisms of Endothelial Dysfunction DOI Open Access
Irakli Kopaliani,

Basant S. M. Elsaid,

Stephan Speier

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(24), P. 13337 - 13337

Published: Dec. 12, 2024

Endothelial dysfunction is a strong prognostic factor in predicting the development of cardiovascular diseases. Dysfunctional endothelium loses its homeostatic ability to regulate vascular tone and prevent overactivation inflammation, leading dysfunction. These functions are critical for homeostasis arterial pressure control, disruption which may lead hypertension. Hypertension itself can also cause endothelial dysfunction, as cells susceptible haemodynamic changes. Although it unclear those factors appear first, they create vicious circle further damaging multiple organs, including heart vessels. There sex-specific differences regarding vessel regulation, contribute blood between men women. Even more importantly, there sex-differences remodelling. Hence, an understanding mechanisms contribution pathological remodelling during hypertension importance. This review addresses immunological metabolic aspects resulting with respect hypertension, potential role differences.

Language: Английский

Citations

3

Ginsenoside Ro prevents endothelial injury via promoting Epac1/AMPK- mediated mitochondria protection in early diabetic retinopathy DOI Creative Commons
Jia Liu, Ying Zhang, Xiaoyu Xu

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 211, P. 107562 - 107562

Published: Dec. 27, 2024

Diabetic retinopathy (DR) is a blinding complication of microangiopathy. First-line therapeutic drugs are all focused on late-stage DR and have several side effects, which could not meet clinical needs. The plant-derived ginsenoside Ro (Ro) has variety effective anti-inflammatory, immune-regulating, cardiovascular protective but its microvascular effects rarely studied. This study aimed to explore the effect mechanism retinal endothelial cells in early stage DR. We demonstrated that exerted cell protection by regulating mitochondrial oxidative stress autophagy AGEs-injured cells. Moreover, alleviated progress through improving thickness pathological changes STZ-induced diabetic mice. Mechanically, promotes activation Epac1-mediated AMPK signaling. On contrary, were abolished Epac1 inhibitor vitro or knock down vivo. Our results revealed important role treatment suggested targeting may be promising approach prevent treat

Language: Английский

Citations

1

NQO1 promotes osteogenesis and suppresses angiogenesis in DPSCs via MAPK pathway modulation DOI Creative Commons
Wanqing Wang, Haoqing Yang,

Zhipeng Fan

et al.

Stem Cell Research & Therapy, Journal Year: 2024, Volume and Issue: 15(1)

Published: Sept. 16, 2024

Influence on stem cells' angiogenesis and osteogenesis of NAD(P)H Quinone Dehydrogenase 1(NQO1) has been established, but its impact dental pulp cells (DPSCs) is unexplored. An important strategy for the treatment arteriosclerosis to inhibit calcium deposition promote vascular repair angiogenesis. This study investigated function mechanism NQO1 DPSCs, so as provide a new ideal arteriosclerosis.

Language: Английский

Citations

0

Mechanosensor Piezo1-Mediated Smooth Muscular Cell Pyroptosis Contributes to Vascular Calcification DOI
Jun Tao,

Daiting You,

Zejiang Feng

et al.

Published: Jan. 1, 2024

Language: Английский

Citations

0