Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis DOI Creative Commons

Peilei Lu,

Danyu Zhang,

Hang Fan

и другие.

Cells, Год журнала: 2023, Номер 12(12), С. 1667 - 1667

Опубликована: Июнь 19, 2023

Pathological cardiac hypertrophy is one of the notable causes heart failure. Circular RNAs (circRNAs) have been studied in association with hypertrophy; however, mechanisms by which circRNAs regulate remain unclear. In this study, we identified a new circRNA, named circCacna1c, hypertrophy. Adult male C57BL/6 mice and H9c2 cells were treated isoprenaline hydrochloride (ISO) to establish model. We found that circCacna1c was upregulated ISO-induced hypertrophic tissue cells. Western blot quantitative real-time polymerase chain reaction showed silencing inhibited gene expression Mechanistically, competitively bound miR-29b-2-5p dual-luciferase reporter assay, downregulated MiR-29b-2-5p nuclear factor activated T cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) control expression. After increased, reduced inhibiting NFATc1 Together, these experiments indicate promotes pathological through miR-29b-2-5p/NFATc1 axis.

Язык: Английский

Effects of SGLT2 inhibitors on ion channels in heart failure: focus on the endothelium DOI Creative Commons
Mengnan Wang, Benedikt Preckel, Coert J. Zuurbier

и другие.

Basic Research in Cardiology, Год журнала: 2025, Номер unknown

Опубликована: Май 14, 2025

Язык: Английский

Процитировано

0
Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease DOI Creative Commons

Naranjan S. Dhalla,

Petr Ošťádal, Paramjit S. Tappia

и другие.

Biomedicines, Год журнала: 2025, Номер 13(6), С. 1338 - 1338

Опубликована: Май 29, 2025

Background: Several mitochondrial abnormalities such as defective energy production, depletion of stores, Ca2+ accumulation, generation reactive oxygen species, and impaired intracellular signaling are associated with cardiac dysfunction during the development different heart diseases. Methods: A narrative review was compiled by a search for applicable literature in MEDLINE via PubMed. Results: Mitochondria generate ATP through processes electron transport oxidative phosphorylation, which is used contractile function. Mitochondria, fact, key subcellular organelle regulation concentration considered to serve buffer maintain homeostasis cardiomyocytes. However, disease, excessive accumulation results mitochondria Ca2+-overload, which, turn, impairs production induces dysfunction. also species (ROS), including superoxide anion radicals hydroxyl well non-radical oxidants hydrogen peroxide, promote lipid peroxidation subsequent disturbance homeostasis, cellular damage, death. Conclusion: These observations support view that both stress Ca2+-overload play critical role disruption pathogenesis pathologies.

Язык: Английский

Процитировано

0
The Ionic Rhodium(Iii) and Iridium(Iii) Complexes of a New 9-Aldehyde Pyrimidylanthrahydrazone Ligand: Synthesis, Crystal Structure and Anticancer Mechanism Studies DOI

J. X. Teng,

Jiayi Li,

Hong-Hua Han

и другие.

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0
Acute activation of SERCA with CDN1163 attenuates IgE ‐mediated mast cell activation through selective impairment of ROS and p38 signaling DOI
Katie D. Hunter, Robert W.E. Crozier, Jessica L. Braun

и другие.

The FASEB Journal, Год журнала: 2023, Номер 37(2)

Опубликована: Янв. 9, 2023

Mast cells are granulocytic immune sentinels present in vascularized tissues that drive chronic inflammatory mechanisms characteristic of allergic pathologies. IgE-mediated mast cell activation leads to a rapid mobilization Ca2+ from intracellular stores, which is essential for the release preformed mediators via degranulation and de novo synthesized proinflammatory cytokines chemokines. Given its potent signaling capacity, dynamics localization highly regulated by various pumps channels controlling cytosolic concentrations. Among these sarco/endoplasmic reticulum -ATPase (SERCA), functions maintain low concentrations actively transporting ions into endoplasmic reticulum. In this study, we characterized role SERCA allergen-activated using IgE-sensitized bone marrow-derived (BMMCs) treated with activating compound, CDN1163, simultaneously stimulated allergen through FcεRI under stem factor (SCF) potentiation. Acute treatment CDN1163 was found attenuate early phase along reactive oxygen species (ROS) production. Additionally, significantly reduced secretion IL-6, IL-13, CCL3, suggesting late response. The protective effects on response may be driven selective suppression p38 MAPK signaling. Together, findings implicate as an important regulator suggest activity offer therapeutic potential targeting pathologies, warranting further investigation.

Язык: Английский

Процитировано

8
Silencing of circCacna1c Inhibits ISO-Induced Cardiac Hypertrophy through miR-29b-2-5p/NFATc1 Axis DOI Creative Commons

Peilei Lu,

Danyu Zhang,

Hang Fan

и другие.

Cells, Год журнала: 2023, Номер 12(12), С. 1667 - 1667

Опубликована: Июнь 19, 2023

Pathological cardiac hypertrophy is one of the notable causes heart failure. Circular RNAs (circRNAs) have been studied in association with hypertrophy; however, mechanisms by which circRNAs regulate remain unclear. In this study, we identified a new circRNA, named circCacna1c, hypertrophy. Adult male C57BL/6 mice and H9c2 cells were treated isoprenaline hydrochloride (ISO) to establish model. We found that circCacna1c was upregulated ISO-induced hypertrophic tissue cells. Western blot quantitative real-time polymerase chain reaction showed silencing inhibited gene expression Mechanistically, competitively bound miR-29b-2-5p dual-luciferase reporter assay, downregulated MiR-29b-2-5p nuclear factor activated T cells, cytoplasmic, calcineurin-dependent 1 (NFATc1) control expression. After increased, reduced inhibiting NFATc1 Together, these experiments indicate promotes pathological through miR-29b-2-5p/NFATc1 axis.

Язык: Английский

Процитировано

8