Activation of Protein Kinase B Rescues against Thapsigargin-Elicited Cardiac Dysfunction through Regulation of NADPH Oxidase and Ferroptosis DOI
Xiaohu Wang, Fengjuan Li, Yong Cheng

et al.

Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: unknown, P. 111292 - 111292

Published: Oct. 1, 2024

Language: Английский

Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia–Reperfusion Injury DOI Creative Commons

Naranjan S. Dhalla,

Petr Ošťádal, Paramjit S. Tappia

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(3), P. 340 - 340

Published: March 14, 2025

Delayed reperfusion of the ischemic heart (I/R) is known to impair recovery cardiac function and produce a wide variety myocardial defects, including ultrastructural damage, metabolic alterations, subcellular Ca2+-handling abnormalities, activation proteases, changes in gene expression. Although I/R injury has been reported induce formation reactive oxygen species (ROS), inflammation, intracellular Ca2+ overload, generation oxidative stress considered play critical role development dysfunction. Increases production superoxide, hydroxyl radicals, oxidants, such as hydrogen peroxide hypochlorous acid, occur hearts subjected injury. In fact, mitochondria are major source excessive ROS due impairment electron transport system well xanthine oxidase NADPH oxidase. Nitric oxide synthase, mainly present endothelium, also activated injury, leading nitric oxide, which, upon combination with superoxide generates nitrosative stress. Alterations function, sarcolemma, sarcoplasmic reticulum activities, mitochondrial phosphorylation, protease simulated exposing oxyradical-generating (xanthine plus oxidase) or H2O2. On other hand, endogenous antioxidants dismutase, catalase, glutathione peroxidase, concentration transcription factor (Nrf2), which modulates expression various antioxidants, depressed hearts. Furthermore, pretreatment catalase N-acetylcysteine, mercaptopropionylglycerine observed attenuate I/R-induced handling Ca2+-regulatory activities; additionally, it found depress improve function. These observations indicate that intimately involved pathological effects different alterations Thus, we faced task developing safe effective agents for upregulating therapy

Language: Английский

Citations

0

Molecular Mechanisms and Therapeutic Targeting of Heat Shock Proteins (HSPs) in Cardiovascular Disorders DOI Creative Commons
Jyoti Upadhyay, Mukesh Nandave, Kamal YT

et al.

Frontiers in Bioscience-Landmark, Journal Year: 2025, Volume and Issue: 30(5)

Published: April 30, 2025

Identifying novel biomarkers is a reliable approach to predict and diagnose human diseases as well manage individual responses therapeutic drugs. Heat shock proteins (HSPs) are molecular chaperones that play major role in maintaining protein stability folding. Many studies suggested their association with multiple types of diseases. HSPs from different categories roles; therefore, it important identify function understand biological functions clearly. This comprehensive review was performed evaluate the predictive cardiovascular The original publications related 2010 2024 were identified by using keywords “heat-shock proteins”, “HSP disorders” atherosclerosis”. regulatory pathways involved HSPs’ functioning points discussion this review. critical key cellular processes, including apoptosis regulation, folding, immune responses, genomic stability, DNA repair. Aberrant expression causes dysregulation these resulting development progression A understanding associated can have significant implications for disease intervention, diagnosis, prognosis. In paper, we highlighted importance versatile targets management

Language: Английский

Citations

0

Activation of Protein Kinase B Rescues against Thapsigargin-Elicited Cardiac Dysfunction through Regulation of NADPH Oxidase and Ferroptosis DOI
Xiaohu Wang, Fengjuan Li, Yong Cheng

et al.

Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: unknown, P. 111292 - 111292

Published: Oct. 1, 2024

Language: Английский

Citations

1