scholarly journals Aerobic exercise ameliorates cardiac hypertrophy by regulating mitochondrial quality control and endoplasmic reticulum stress through M 2 AChR

2021 ◽  
Author(s):  
Mei Ma ◽  
Wei Chen ◽  
Yijie Hua ◽  
Hao Jia ◽  
Yinping Song ◽  
...  
Keyword(s):  
Quality Control ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Hypertrophy ◽  
Aerobic Exercise ◽  
Mitochondrial Quality Control

The roles of mitochondria-associated membranes in mitochondrial quality control under endoplasmic reticulum stress

Life Sciences ◽  
2019 ◽  
Vol 231 ◽  
pp. 116587 ◽  
Author(s):  
Beiwu Lan ◽  
Yichun He ◽  
Hongyu Sun ◽  
Xinzi Zheng ◽  
Yufei Gao ◽  
...  
Keyword(s):  
Quality Control ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Quality Control

scholarly journals Endoplasmic Reticulum Stress is Involved in DFMO Attenuating Isoproterenol-Induced Cardiac Hypertrophy in Rats

2016 ◽  
Vol 38 (4) ◽  
pp. 1553-1562 ◽  
Author(s):  
Yan Lin ◽  
Xiaojie Zhang ◽  
Wei Xiao ◽  
Bo Li ◽  
Jun Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Cardiac Fibrosis ◽  
Regulation Of Gene Expression ◽  
Tunel Staining

Background/Aims: Studies performed in experimental animals have shown that polyamines contribute to several physiological and pathological processes, including cardiac hypertrophy. This involves an increase in ornithine decarboxylase (ODC) activity and intracellular polyamines associated with regulation of gene expression. Difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, has attracted considerable interest for its antiproliferative role, which it exerts through inhibition of the polyamine pathway and cell turnover. Whether DFMO attenuates cardiac hypertrophy through endoplasmic reticulum stress (ERS) is unclear. Methods: Myocardial hypertrophy was simulated by isoproterenol (ISO). Polyamine depletion was achieved using DFMO. Hypertrophy was estimated using the heart/body index and atrial natriuretic peptide (ANP) gene expression. Cardiac fibrosis and apoptosis were measured by Masson and TUNEL staining. Expression of ODC and spermidine/spermine N1-acetyltransferase (SSAT) were analyzed via real-time PCR and Western blot analysis. Protein expression of ERS and apoptosis factors were analyzed using Western blot analysis. Results: DFMO treatments significantly attenuated hypertrophy and apoptosis induced by ISO in cardiomyocytes. DFMO down-regulated the expression of ODC, glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), cleaved caspase-12, and Bax and up-regulated the expression of SSAT and Bcl-2. Finally, these changes were partially reversed by the addition of exogenous putrescine. Conclusion: The data presented here suggest that polyamine depletion could inhibit cardiac hypertrophy and apoptosis, which is closely related to the ERS pathway.

The influence of aerobic exercise on mitochondrial quality control in skeletal muscle

2021 ◽  
Author(s):  
Ashleigh M. Philp ◽  
Nicholas J. Saner ◽  
Michael Lazarou ◽  
Ian G. Ganley ◽  
Andrew Philp
Keyword(s):  
Skeletal Muscle ◽  
Quality Control ◽  
Aerobic Exercise ◽  
Mitochondrial Quality Control

The role of MicroRNAs on endoplasmic reticulum stress in myocardial ischemia and cardiac hypertrophy

2019 ◽  
Vol 150 ◽  
pp. 104516 ◽  
Author(s):  
Navid Omidkhoda ◽  
A. Wallace Hayes ◽  
Russel J. Reiter ◽  
Gholamreza Karimi
Keyword(s):  
Endoplasmic Reticulum ◽  
Myocardial Ischemia ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Hypertrophy

scholarly journals PERK MEDIATED ENDOPLASMIC RETICULUM STRESS IS INVOLVED IN ANGIOTENSINIIINDUCED CARDIAC HYPERTROPHY

Heart ◽  
2012 ◽  
Vol 98 (Suppl 2) ◽  
pp. E112.1-E112 ◽  
Author(s):  
Lu Zhen-Rong ◽  
Wang Xiao-Reng ◽  
Li Yu-Zhen ◽  
Wang Chen ◽  
Liu Xiu-Hua
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cardiac Hypertrophy

scholarly journals Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) and Their Prospective Roles in Kidney Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-21
Author(s):  
Peng Gao ◽  
Wenxia Yang ◽  
Lin Sun
Keyword(s):  
Quality Control ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Er Stress ◽  
Future Research ◽  
Inflammasome Activation ◽  
Mitochondrial Quality Control ◽  
Downstream Signaling ◽  
Contact Sites ◽  
Progression Of Kidney Disease

Mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) serve as essential hubs for interorganelle communication in eukaryotic cells and play multifunctional roles in various biological pathways. A defect in ER-mitochondria signaling or MAMs dysfunction has pleiotropic effects on a variety of intracellular events, which results in disturbances of the mitochondrial quality control system, Ca2+ dyshomeostasis, apoptosis, ER stress, and inflammasome activation, which all contribute to the onset and progression of kidney disease. Here, we review the structure and molecular compositions of MAMs as well as the experimental methods used to study these interorganellar contact sites. We will specifically summarize the downstream signaling pathways regulated by MAMs, mainly focusing on mitochondrial quality control, oxidative stress, ER-mitochondria Ca2+ crosstalk, apoptosis, inflammasome activation, and ER stress. Finally, we will discuss how alterations in MAMs integrity contribute to the pathogenesis of kidney disease and offer directions for future research.

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