Cardiovascular disease (CVD) is one of the leading causes of mortality in humans, and oxidative stress plays a pivotal role in disease progression. This phenomenon typically arises from weakening of the cellular antioxidant system or excessive accumulation of peroxides. This review focuses on a specialized form of oxidative stress-disulfide stress-which is triggered by an imbalance in the glutaredoxin and thioredoxin antioxidant systems within the cell, leading to the accumulation of disulfide bonds. The genesis of disulfide stress is usually induced by extrinsic pathological factors that disrupt the thiol-dependent antioxidant system, manifesting as sustained glutathionylation of proteins, formation of abnormal intermolecular disulfide bonds between cysteine-rich proteins, or irreversible oxidation of thiol groups to sulfenic and sulfonic acids. Disulfide stress not only precipitates the collapse of the antioxidant system and the accumulation of reactive oxygen species, exacerbating oxidative stress, but may also initiate cellular inflammation, autophagy, and apoptosis through a cascade of signaling pathways. Furthermore, this review explores the detrimental effects of disulfide stress on the progression of various CVDs including atherosclerosis, hypertension, myocardial ischemia-reperfusion injury, diabetic cardiomyopathy, cardiac hypertrophy, and heart failure. This review also proposes several potential therapeutic avenues to improve the future treatment of CVDs.
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http://dx.doi.org/10.1016/j.redox.2024.103297 | DOI Listing |
J Biol Chem
December 2024
Department of Cell and Molecular Physiology, Loyola University Chicago, Maywood, IL, USA. Electronic address:
The sarco(endo)plasmic reticulum Ca ATPase (SERCA) is a membrane transporter that creates and maintains intracellular Ca stores. In the heart, SERCA is regulated by an inhibitory interaction with the monomeric form of the transmembrane micropeptide phospholamban (PLB). PLB also forms avid homo-pentamers, and dynamic exchange of PLB between pentamers and SERCA is an important determinant of cardiac responsiveness to exercise.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2024
Department of Internal Medicine 1, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo, Shimane, 693-8501, Japan; The Center for Integrated Kidney Research and Advance, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo, 693-8501, Japan. Electronic address:
Inhibition of xanthine oxidoreductase (XOR) was shown to ameliorate the stroke susceptibility in the stroke-prone spontaneously hypertensive rat (SHRSP), suggesting hyperuricemia had a pathological role in this rat model. In this study, we thus aimed to explore mechanisms inducing hyperuricemia in SHRSP. XOR is known to have two forms, xanthine dehydrogenase (XDH) as the prototype and xanthine oxidase (XO) as the converted form through cleavage of a peptide bond or through formation of disulfide bonds in the enzyme.
View Article and Find Full Text PDFInt J Gynaecol Obstet
December 2024
Department of Gynecology and Obstetrics, University of Health Sciences Ankara City Hospital, Ankara, Turkey.
Objective: The aim is to contrast the serum levels of thiol-disulfide homeostasis and ischemic modified albumin between patients with leiomyoma and healthy individuals and to assess the impact of oxidative stress on the etiopathogenesis of leiomyoma.
Methods: In this prospective case-control study, a total of 154 participants were included, consisting of 77 cases diagnosed with leiomyoma and 77 healthy individuals without leiomyoma. The demographic characteristics and ultrasonographic findings of the participants were recorded, and parameters such as albumin, ischemia-modified albumin, and thiol-disulfide homeostasis were evaluated.
Artif Cells Nanomed Biotechnol
December 2025
Head and Neck Surgery, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, China.
Gastric cancer remains one of the deadliest cancers globally due to delayed detection and limited treatment options, underscoring the critical need for innovative prognostic methods. Disulfidptosis, a recently discovered programmed cell death triggered by disulphide stress, presents a fresh avenue for therapeutic exploration. This research examines disulfidptosis-related long noncoding RNAs (DRLs) in gastric cancer, with the goal of leveraging these lncRNAs as potential markers to enhance patient outcomes and treatment approaches.
View Article and Find Full Text PDFTransl Cancer Res
November 2024
Department of Breast Care Surgery, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Background: Disulfidptosis is a novel form of cell death triggered by disulfide stress that may have important implications for breast cancer (BC) pathogenesis. Nevertheless, studies identifying disulfidptosis-associated long non-coding RNAs (lncRNAs) in BC have not been reported. This study aimed to investigate the prognostic potential of disulfidptosis-related lncRNAs in BC.
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