PATHOGENIC MECHANISMS OF HEART FAILURE IN PATIENTS WITH TYPE 2 DIABETES MELLITUS DOI Creative Commons
В. С. Иванченко, А. А. Гагарина,

I. Ya. Goryanskaya

et al.

Complex Issues of Cardiovascular Diseases, Journal Year: 2023, Volume and Issue: 12(4S), P. 162 - 172

Published: Dec. 29, 2023

Highlights The review presents up-to-date data on the contribution of type 2 diabetes mellitus to development and progression heart failure. highlights key mechanisms pathogenesis failure associated with changes in energy metabolism cardiomyocytes. Abstract Type is one main risk factors that significantly worsen prognosis increases probability fatal cardiovascular events. diabetic patients involves a great number for rapid atherosclerosis, as well numerous combinations neurohumoral, molecular histological not atherogenesis, which interconnection results complications decompensation. This discusses underlying mellitus, particular, special attention paid cardiomyocyte metabolism, death, significance epigenetic chronic

Language: Английский

AMPK and O-GlcNAcylation: interplay in cardiac pathologies and heart failure DOI

E. Vanni,

C Beauloye,

Sandrine Horman

et al.

Essays in Biochemistry, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 25, 2024

Abstract Heart failure (HF) represents a multifaceted clinical syndrome characterized by the heart’s inability to pump blood efficiently meet body’s metabolic demands. Despite advances in medical management, HF remains major cause of morbidity and mortality worldwide. In recent years, considerable attention has been directed toward understanding molecular mechanisms underlying pathogenesis, with particular focus on role AMP-activated protein kinase (AMPK) O-GlcNAcylation. This review comprehensively examines current AMPK O-GlcNAcylation signalling pathways HF, emphasizing their interplay dysregulation. We delve into intricate which contribute cardiac energetics, metabolism, remodelling, highlighting preclinical studies that have explored novel therapeutic interventions targeting these pathways.

Language: Английский

Citations

2

Can O-GIcNAc Transferase (OGT) Complex Be Used as a Target for the Treatment of Hematological Malignancies? DOI Creative Commons

Shiwei Zhuang,

Zhimei Liu, Jinyao Wu

et al.

Pharmaceuticals, Journal Year: 2024, Volume and Issue: 17(6), P. 664 - 664

Published: May 22, 2024

The circulatory system is a closed conduit throughout the body and consists of two parts as follows: cardiovascular lymphatic system. Hematological malignancies usually grow multiply in system, directly or indirectly affecting its function. These include multiple myeloma, leukemia, lymphoma. O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) regulates function stability substrate proteins through O-GlcNAc modification. Abnormally expressed OGT strongly associated with tumorigenesis, including hematological malignancies, colorectal cancer, liver breast prostate cancer. In cells, can assemble variety to form complexes exercise related biological functions, such OGT/HCF-1, OGT/TET, NSL, then regulate glucose metabolism, gene transcription, cell proliferation, other processes, thus development malignancies. This review summarizes involved assembly cells role Unraveling complex network regulated by will facilitate better understanding hematologic malignancy progression.

Language: Английский

Citations

1

Alarin moderated myocardial hypertrophy via inhibiting cyclic adenosine monophosphate/protein kinase A signaling pathway to attenuate autophagy DOI
Tongtong Shen, Yu Liu, Shuangshuang Dong

et al.

Peptides, Journal Year: 2021, Volume and Issue: 146, P. 170669 - 170669

Published: Oct. 6, 2021

Language: Английский

Citations

8

The Regulatory Mechanism and Effect of RIPK3 on PE-induced Cardiomyocyte Hypertrophy DOI
Xue Wang, Jingjing Zhang,

Jianan Qian

et al.

Journal of Cardiovascular Pharmacology, Journal Year: 2022, Volume and Issue: 80(2), P. 236 - 250

Published: May 13, 2022

Abstract: As a critical regulatory molecule, receptor-interacting protein kinase 3 (RIPK3) can mediate the signaling pathway of programmed necrosis. Calcium/calmodulin-dependent II (CaMKII) has been proved as new substrate for RIPK3-induced necroptosis. In this study, we aimed to investigate mechanism RIPK3 on phenylephrine (PE)-induced cardiomyocyte hypertrophy. Cardiomyocyte hypertrophy was induced by exposure PE (100 μM) 48 hours. Primary cardiomyocytes were pretreated with inhibitor GSK′872 (10 μM), and siRNA used deplete intracellular expression RIPK3. The indexes related myocardial hypertrophy, cell injury, necroptosis, CaMKII activation, gene expression, oxidative stress, mitochondrial membrane potential measured. We found that after stimulated PE, expressions markers, atrial brain natriuretic peptides (ANP BNP), increased, release lactate dehydrogenase level adenosine triphosphate (ATP) decreased, oxidation phosphorylation levels CaMKIIδ alternative splicing disturbed. However, both depletion could reduce dysfunction, inhibit activation finally alleviate addition, pretreatment also lessen accumulation reactive oxygen species (ROS) stabilize mitochondria. These results indicated targeted inhibition suppress necroptosis leading alleviated Collectively, our findings provided valuable insights into clinical treatment hypertrophic cardiomyopathy.

Language: Английский

Citations

6

Perilipin 5 deficiency aggravates cardiac hypertrophy by stimulating lactate production in leptin-deficient mice DOI Creative Commons

Lele Jian,

Xing Gao, Chao Wang

et al.

Biology Direct, Journal Year: 2023, Volume and Issue: 18(1)

Published: Sept. 4, 2023

Abstract Background Perilipin 5 (Plin5) is well known to maintain the stability of intracellular lipid droplets (LDs) and regulate fatty acid metabolism in oxidative tissues. It highly expressed heart, but its roles have yet be fully elucidated. Methods Plin5-deficient mice Plin5/leptin-double-knockout were produced, their histological structures myocardial functions observed. Critical proteins related glucose measured heart tissues, neonatal mouse cardiomyocytes Plin5-overexpressing H9C2 cells. 2-NBDG was employed detect uptake. The mitochondria contents observed by MitoTracker BODIPY 493/503 staining cardiomyocytes. Results Plin5 deficiency impaired utilization caused insulin resistance cardiomyocytes, particularly presence acids (FAs). Additionally, increased NADH content elevated expression lactate dehydrogenase (LDHA) which resulted production. Moreover, when oxidation blocked etomoxir or LDHA inhibited GSK2837808A improved. Leptin-deficient exhibited hypertrophy, altered substrate utilization, exacerbated hypertrophy leptin-deficient mice. Conclusion Our results demonstrated that plays a critical role coordinating providing potential target for treatment metabolic disorders heart. Graphic abstract

Language: Английский

Citations

3

Perm1 Regulates Mitochondrial Energetics Through O-Glcnacylation in the Heart DOI
Karthi Sreedevi,

Amina James,

Sara Do

et al.

Published: Jan. 1, 2024

Download This Paper Open PDF in Browser Add to My Library Share: Permalink Using these links will ensure access this page indefinitely Copy URL DOI

Language: Английский

Citations

0

PERM1 regulates mitochondrial energetics through O-GlcNAcylation in the heart DOI
Karthi Sreedevi,

Amina James,

Sara Do

et al.

Journal of Molecular and Cellular Cardiology, Journal Year: 2024, Volume and Issue: 198, P. 1 - 12

Published: Nov. 23, 2024

Language: Английский

Citations

0

PATHOGENIC MECHANISMS OF HEART FAILURE IN PATIENTS WITH TYPE 2 DIABETES MELLITUS DOI Creative Commons
В. С. Иванченко, А. А. Гагарина,

I. Ya. Goryanskaya

et al.

Complex Issues of Cardiovascular Diseases, Journal Year: 2023, Volume and Issue: 12(4S), P. 162 - 172

Published: Dec. 29, 2023

Highlights The review presents up-to-date data on the contribution of type 2 diabetes mellitus to development and progression heart failure. highlights key mechanisms pathogenesis failure associated with changes in energy metabolism cardiomyocytes. Abstract Type is one main risk factors that significantly worsen prognosis increases probability fatal cardiovascular events. diabetic patients involves a great number for rapid atherosclerosis, as well numerous combinations neurohumoral, molecular histological not atherogenesis, which interconnection results complications decompensation. This discusses underlying mellitus, particular, special attention paid cardiomyocyte metabolism, death, significance epigenetic chronic

Language: Английский

Citations

0