BDNF mimetics recover palmitic acid-induced injury in cardiomyocytes by ameliorating Akt-dependent mitochondrial impairments DOI

Man-ru Zhang,

Bang-Yun Zuo,

Yu-Chen Song

и другие.

Toxicology and Applied Pharmacology, Год журнала: 2024, Номер 486, С. 116951 - 116951

Опубликована: Май 1, 2024

Язык: Английский

Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise DOI
Xinxin Cui, Michail Spanos, Cuimei Zhao

и другие.

Journal of Cardiovascular Translational Research, Год журнала: 2025, Номер unknown

Опубликована: Янв. 25, 2025

Язык: Английский

Процитировано

2

Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment DOI Creative Commons
Yong Liu,

Jin-Ling Huo,

Kaidi Ren

и другие.

Cell Death Discovery, Год журнала: 2024, Номер 10(1)

Опубликована: Март 20, 2024

Abstract Diabetic cardiomyopathy (DCM), an important complication of diabetes mellitus (DM), is one the most serious chronic heart diseases and has become a major cause failure worldwide. At present, pathogenesis DCM unclear, there still lack effective therapeutics. Previous studies have shown that homeostasis mitochondria endoplasmic reticulum (ER) play core role in maintaining cardiovascular function, structural functional abnormalities these organelles seriously impact occurrence development various diseases, including DCM. The interplay between ER mediated by mitochondria-associated membrane (MAM), which participates regulating energy metabolism, calcium homeostasis, mitochondrial dynamics, autophagy, stress, inflammation, other cellular processes. Recent proven MAM closely related to initiation progression In this study, we aim summarize recent research progress on MAM, elaborate key DCM, discuss potential as therapeutic target for thereby providing theoretical reference basic clinical treatment.

Язык: Английский

Процитировано

12

Hyperglycemia triggers RyR2-dependent alterations of mitochondrial calcium homeostasis in response to cardiac ischemia-reperfusion: Key role of DRP1 activation DOI Creative Commons

Mathilde Dubois,

Doria Boulghobra,

Gilles Rochebloine

и другие.

Redox Biology, Год журнала: 2024, Номер 70, С. 103044 - 103044

Опубликована: Янв. 19, 2024

Hyperglycemia increases the heart sensitivity to ischemia-reperfusion (IR), but underlying cellular mechanisms remain unclear. Mitochondrial dynamics (the processes that govern mitochondrial morphology and their interactions with other organelles, such as reticulum), has emerged a key factor in vulnerability IR. However, it is unknown whether contributes hyperglycemia deleterious effect during We hypothesized (i) higher IR hyperglycemic conditions could be explained by on complex interplay between dynamics, Ca

Язык: Английский

Процитировано

10

The correlation between mitochondria-associated endoplasmic reticulum membranes (MAMs) and Ca2+ transport in the pathogenesis of diseases DOI
Wenbin Zhao, Rui Sheng

Acta Pharmacologica Sinica, Год журнала: 2024, Номер unknown

Опубликована: Авг. 8, 2024

Язык: Английский

Процитировано

10

Upregulation of NF-κB by USP24 aggravates ferroptosis in diabetic cardiomyopathy DOI Creative Commons
Shenglin Wu,

Yueran Zhou,

Jiaquan Liang

и другие.

Free Radical Biology and Medicine, Год журнала: 2023, Номер 210, С. 352 - 366

Опубликована: Дек. 5, 2023

Recent investigations have proposed a potential causal association between the occurrence of ferroptosis, nuclear factor kappa B (NF-κB) and ubiquitin-specific protease 24 (USP24). Nevertheless, mechanism USP24 NF-κB regulation ferroptosis in context diabetic cardiomyopathy (DCM) remain unclear. In this study, high-fat diet streptozotocin-induced mouse DCM model were established, high glucose palmitic acid treatment H9c2 cells neonatal primary cardiomyocytes (NMPCs) was used as an vitro models. Utilizing both vivo models, we assessed USP24, NF-κB, levels, explored relationship among them. increased expression phosphorylated (p–NF–κB) fatty acid-CoA ligase 4 (FACL4) detected, along with accumulated iron, well reduced ferritin heavy chain 1 (FTH1), solute carrier family 7 member 11 (SLC7A11) antioxidant capacity. Knockdown resulted reduction while knockdown did not lead to decrease expression. Moreover, cells, separately levels FACL4, SLC7A11 FTH1, improved capacity cell viability. shUSP24 administration phorbol 12-myristate 13-acetate (PMA) activated subsequently reversing previously observed effect caused by knockdown. These findings show that upregulates promote DCM.

Язык: Английский

Процитировано

16

Single-cell insights: pioneering an integrated atlas of chromatin accessibility and transcriptomic landscapes in diabetic cardiomyopathy DOI Creative Commons
Qiang Su, Wanzhong Huang, Yu‐An Huang

и другие.

Cardiovascular Diabetology, Год журнала: 2024, Номер 23(1)

Опубликована: Апрель 25, 2024

Diabetic cardiomyopathy (DCM) poses a growing health threat, elevating heart failure risk in diabetic individuals. Understanding DCM is crucial, with fibroblasts and endothelial cells playing pivotal roles driving myocardial fibrosis contributing to cardiac dysfunction. Advances Multimodal single-cell profiling, such as scRNA-seq scATAC-seq, provide deeper insights into DCM's unique cell states molecular landscape for targeted therapeutic interventions.

Язык: Английский

Процитировано

6

Suppression of RCAN1 alleviated lipid accumulation and mitochondrial fission in diabetic cardiomyopathy DOI Creative Commons
Songren Shu, Hao Cui, Zirui Liu

и другие.

Metabolism, Год журнала: 2024, Номер 158, С. 155977 - 155977

Опубликована: Июль 23, 2024

Although metabolic disturbance is a characteristic of diabetic cardiomyopathy (DbCM), the detailed pathogenesis DbCM remains unknown.

Язык: Английский

Процитировано

6

BMAL1 ameliorates type 2 diabetes-induced cognitive impairment via AREG upregulation and PI3K/Akt/GSK-3β pathway activation DOI Creative Commons
Jialu Xu,

Chunyu Li,

Rongping Fan

и другие.

Cell Communication and Signaling, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 6, 2025

Cognitive impairment is a significant complication of type 2 diabetes mellitus (T2DM). However, the mechanisms underlying development cognitive dysfunction in individuals with T2DM remain elusive. Herein, we discussed role Bmal1, core circadian rhythm-regulating gene, process T2DM-associated dysfunction. We identified marked decrease BMAL1 levels hippocampus db/db mice, followed by gain- and loss-of-function studies to explore impact on function. Our findings indicated that downregulation led deficits, characterized tau hyperphosphorylation accumulated amyloid plaque. Conversely, overexpression mitigated these Alzheimer-like pathologies. Further investigation revealed directly activated transcription Areg, thereby activating PI3K/Akt/GSK-3β pathway ameliorating Moreover, effects were attenuated LY294002, PI3K inhibitor. Collectively, results underscore impairment, proposing novel intervention strategy for exposed risk factors T2DM.

Язык: Английский

Процитировано

0

Macrod1 suppresses diabetic cardiomyopathy via regulating PARP1-NAD+-SIRT3 pathway DOI
Yuting Liu,

Hong-liang Qiu,

Hongxia Xia

и другие.

Acta Pharmacologica Sinica, Год журнала: 2024, Номер 45(6), С. 1175 - 1188

Опубликована: Март 8, 2024

Язык: Английский

Процитировано

4

Mitochondrial energy metabolism in diabetic cardiomyopathy: Physiological adaption, pathogenesis, and therapeutic targets DOI Creative Commons

Wanlin Ye,

Kun Han,

Maodi Xie

и другие.

Chinese Medical Journal, Год журнала: 2024, Номер 137(8), С. 936 - 948

Опубликована: Март 25, 2024

Abstract Diabetic cardiomyopathy is defined as abnormal structure and function of the heart in setting diabetes, which could eventually develop failure leads to death patients. Although blood glucose control medications show beneficial effects on this disease, there currently no specific treatment for diabetic cardiomyopathy. Over past few decades, pathophysiology has been extensively studied, an increasing number studies pinpoint that impaired mitochondrial energy metabolism a key mediator well therapeutic target. In review, we summarize latest research field cardiomyopathy, focusing damage adaptation, altered substrates, potential targets. A better understanding may help gain more mechanistic insights generate precise mitochondria-oriented therapies treat disease.

Язык: Английский

Процитировано

4