High Salt Exacerbates Myocardial Dysfunction In Vitro and In Vivo by Promoting SIRT1/Nrf2‐Mediated Ferroptosis DOI

Wu Guanji,

Fuqiang Liu,

You Fei

и другие.

Clinical and Experimental Pharmacology and Physiology, Год журнала: 2024, Номер 52(2)

Опубликована: Дек. 29, 2024

Myocardial dysfunction is a crucial determinant of the development heart failure in salt-sensitive hypertension. Ferroptosis, programmed iron-dependent cell death, has been increasingly recognised as an important contributor to pathophysiology various cardiovascular diseases. This study aims investigate role and underlying mechanism ferroptosis high-salt (HS)-induced myocardial damage. Our results reveal that HS stimulation inhibited proliferation promoted apoptosis cardiomyocyte HL-1 cells dose-dependent manner. Ferroptotic features were observed HS-induced cells, including ferric iron accumulation, decreased glutathione levels, increased oxidative stress upregulation marker proteins PTGS2, 4HNE FTH1 downregulation GPX4, all which reversed by treatment with suppressor Fer-1. Furthermore, administration Fer-1 ameliorated damage Dahl SS rats. Additionally, we found diet suppressed SIRT1/Nrf2 signalling pathway activation our vivo experiments. Activation SIRT1 overexpression significantly attenuated cells. In conclusion, findings demonstrate levels induce injury promoting via deactivation pathway, highlighting potential for therapeutic targeting hypertension-related disorders.

Язык: Английский

High-intensity training on CREB activation for improving brain health: a narrative review of possible molecular talks DOI Creative Commons
Ping Li,

Yan Hu,

Liqi Tong

и другие.

Frontiers in Endocrinology, Год журнала: 2025, Номер 15

Опубликована: Янв. 20, 2025

Although physical exercise has obvious benefits in brain physiology, the molecular biomarkers induced by protocols are inconclusive. Evidence indicates that interventions effective shaping physiology. However, potential mediator for improving functions is uncertain. CREB one of targets triggers various cross-talk to improve neurogenesis, long-term potentiation, and synaptogenesis. Therefore, may be situated on causal path between maintaining health exercising. To support this, studies have shown exercise-mediated phosphorylation improves cognitive memory. In addition, among (types, duration, frequency), intensity been reported most triggering CREB-mediated signaling. For example, HIT increases synthesis CREB, which not only induce physiology but also pathology higher activation its downstream targets, such as BDNF. this review aims understand effects function how can mediate CREB-induced health.

Язык: Английский

Процитировано

1
Oxidative Stress in Brain Function DOI Creative Commons

Daniela-Marilena Trofin,

Dragos-Petrica Sardaru,

Dan Trofin

и другие.

Antioxidants, Год журнала: 2025, Номер 14(3), С. 297 - 297

Опубликована: Фев. 28, 2025

Oxidative stress (OS) is an important factor in the pathophysiology of numerous neurodegenerative disorders, such as Parkinson's disease, multiple sclerosis, cerebrovascular pathology or Alzheimer's disease. OS also significantly influences progression among various disorders. The imbalance between formation reactive oxygen species (ROS) and body's capacity to neutralize these toxic byproducts renders brain susceptible oxidative injury. Increased amounts ROS can result cellular malfunction, apoptosis neurodegeneration. They represent a substantial mitochondrial dysfunction, defining characteristic Comprehending fundamental mechanisms its interactions with function, neuroinflammation protective pathways becomes essential for formulating targeted therapeutics maintain health reduce impacts We address recent highlights on role function terms significance neuronal

Язык: Английский

Процитировано

1
Lactate Mediates Exercise-Induced Modulation of Mitophagy and Ferroptosis, Reducing Amyloid-Beta and Tau in Type 2 Diabetes: A Molecular Study DOI
Kayvan Khoramipour,

Pouria Khosravi,

Fereshteh Shahidi

и другие.

Опубликована: Янв. 1, 2025

Background: This study examined the impact of lactate accumulation, induced by high-intensity interval training (HIIT), on reducing amyloid-beta (Aβ) and tau protein levels through enhanced mitophagy decreased ferroptosis in hippocampus type 2 diabetic rats.Methods: Thirty-two male Wistar rats were divided into four groups: control (Co), exercise (EX), diabetes (DB), with (DB + EX). Diabetes was DB EX groups via a high-fat diet followed streptozotocin injection (35 mg/kg). The performed treadmill-based HIIT, involving 4–10 running intervals at 80–100% Vmax. Serum hippocampal expression MCT2, SIRT1, BDNF, p62, Keap1, NRF2, MDA, GPX4, PINK1, parkin, Aβ, Tau assessed.Results: In group, Parkin elevated, while reduced compared to group.Conclusion: HIIT enhances reduces lactate-SIRT1-BDNF p62-Keap1-NRF2 pathways, potentially mitigating Aβ accumulation.

Язык: Английский

Процитировано

0
Intercellular Adhesion Molecule 1 (ICAM-1): An Inflammatory Regulator with Potential Implications in Ferroptosis and Parkinson’s Disease DOI Creative Commons
Matthew Miller,

Harold E. Landis,

Robert E. Miller

и другие.

Cells, Год журнала: 2024, Номер 13(18), С. 1554 - 1554

Опубликована: Сен. 15, 2024

Intercellular adhesion molecule 1 (ICAM-1/CD54), a transmembrane glycoprotein, has been considered as one of the most important molecules during leukocyte recruitment. It is encoded by ICAM1 gene and plays central role in inflammation. Its crucial many inflammatory diseases such ulcerative colitis rheumatoid arthritis are well established. Given that neuroinflammation, underscored microglial activation, key element neurodegenerative Parkinson’s disease (PD), we investigated whether ICAM-1 this progressive neurological condition and, if so, to elucidate underpinning mechanisms. Specifically, were interested potential interaction between ICAM-1, glial cells, ferroptosis, an iron-dependent form cell death recently implicated PD. We conclude there exist direct indirect (via cells T cells) influences on ferroptosis further elucidation these interactions can suggest novel intervention for devastating disease.

Язык: Английский

Процитировано

2
Physical exercise-mediated neuroprotective mechanisms in Parkinson's disease, Alzheimer's disease, and epilepsy DOI Creative Commons
Ricardo A. Pinho, A. Müller, Luis Felipe Marqueze

и другие.

Brazilian Journal of Medical and Biological Research, Год журнала: 2024, Номер 57

Опубликована: Янв. 1, 2024

Research suggests that physical exercise is associated with prevention and management of chronic diseases. The influence on brain function metabolism the mechanisms involved are well documented in literature. This review provides a comprehensive overview potential implications molecular benefits Parkinson's disease, Alzheimer's epilepsy. Here, we present an effects various aspects function. To this end, conducted extensive literature search PubMed, Web Science, Google Scholar databases to identify articles published past two decades. delves into key including modulation neuroinflammation, neurotrophic factors, synaptic plasticity. Moreover, explored role advancing therapeutic strategies for these In conclusion, highlights importance regular as complementary non-pharmacological treatment individuals neurological disorders such Alzheimer's,

Язык: Английский

Процитировано

1
Irisin Attenuates Neuroinflammation Targeting the NLRP3 Inflammasome DOI Creative Commons
Francesca Martina Filannino, Melania Ruggiero, Maria Antonietta Panaro

и другие.

Molecules, Год журнала: 2024, Номер 29(23), С. 5623 - 5623

Опубликована: Ноя. 28, 2024

Neuroinflammation is defined as an immune response involving various cell types, particularly microglia, which monitor the neuroimmune axis. Microglia activate in two distinct ways: M1, pro-inflammatory and capable of inducing phagocytosis releasing factors, M2, has anti-inflammatory properties. Inflammasomes are large protein complexes that form to internal danger signals, activating caspase-1 leading release cytokines such interleukin 1β. Irisin, a peptide primarily released by muscles during exercise, was examined for its effects on BV2 microglial cells vitro. Even at low concentrations, irisin observed influence NLRP3 inflammasome, showing potential neuroprotective agent after stimulation with lipopolysaccharides (LPSs). Irisin helped maintain microglia their typical physiological state reduced migratory capacity. also increased Arg-1 expression, marker M2 polarization, while downregulating NLRP3, Pycard, caspase-1, IL-1β, CD14. The results this study indicate may serve crucial mediator neuroprotection, thus representing innovative tool prevention neurodegenerative diseases.

Язык: Английский

Процитировано

0
High Salt Exacerbates Myocardial Dysfunction In Vitro and In Vivo by Promoting SIRT1/Nrf2‐Mediated Ferroptosis DOI

Wu Guanji,

Fuqiang Liu,

You Fei

и другие.

Clinical and Experimental Pharmacology and Physiology, Год журнала: 2024, Номер 52(2)

Опубликована: Дек. 29, 2024

Myocardial dysfunction is a crucial determinant of the development heart failure in salt-sensitive hypertension. Ferroptosis, programmed iron-dependent cell death, has been increasingly recognised as an important contributor to pathophysiology various cardiovascular diseases. This study aims investigate role and underlying mechanism ferroptosis high-salt (HS)-induced myocardial damage. Our results reveal that HS stimulation inhibited proliferation promoted apoptosis cardiomyocyte HL-1 cells dose-dependent manner. Ferroptotic features were observed HS-induced cells, including ferric iron accumulation, decreased glutathione levels, increased oxidative stress upregulation marker proteins PTGS2, 4HNE FTH1 downregulation GPX4, all which reversed by treatment with suppressor Fer-1. Furthermore, administration Fer-1 ameliorated damage Dahl SS rats. Additionally, we found diet suppressed SIRT1/Nrf2 signalling pathway activation our vivo experiments. Activation SIRT1 overexpression significantly attenuated cells. In conclusion, findings demonstrate levels induce injury promoting via deactivation pathway, highlighting potential for therapeutic targeting hypertension-related disorders.

Язык: Английский

Процитировано

0