Research Progress on the Interaction Between Autophagy and Energy Homeostasis in Cardiac Remodeling

Ding, Wen; Hong, Feng; Li, Wenjing; Liao, Hai-Han; Tang, Qi‐Zhu

doi:10.3389/fphar.2020.587438

Cited by 11 publications

(6 citation statements)

References 97 publications

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“…Rats exposed to daily T4 treatment for 4 weeks exhibited hyperthyroid (HT) status as manifested by increased serum free T3 and T4 concentrations as well as marked weight loss. This experimentally induced hyperthyroidism rapidly induced cardiomyopathy as evidenced by marked increases in HR, SBP, and LVESP, and further examination revealed multiple signs indicative of myocardial hypertrophy, including greater dry heart/body weight ratio 16 , elevated serum concentrations of NT-proBNP and FGF-23, myocardial upregulation of the remodeling marker MMP-9, collagen fiber accumulation 17 , and upregulation of various fibrotic marker genes and the regulatory miRNA let-7b 18 . It is well documented that increased TH levels enhance HR and cardiac output through activation of the SNS and RAS among other mechanisms 19 , leading to myocardial hypertrophy 5 .…”

Section: Discussionmentioning

confidence: 97%

“…These changes were also reversed by valsartan and LCZ696 27 , possibly by normalizing miR-377 expression and causing a rebound increase in autophagy 7 , 24 . In turn, upregulation of autophagy by these agents could reduce pathological cardiac remodeling by enhancing energy balance, nutrient reserves, and amino acid reserves 16 . Consistent with this notion, the CH group also exhibited significant downregulation of the myocardial metabolic regulator PPAR-ϒ 17 , and this decrease was similarly reversed by valsartan and to a greater extent by LCZ696.…”

Section: Discussionmentioning

confidence: 99%

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Sacubitril/valsartan (LCZ696) ameliorates hyperthyroid-induced cardiac hypertrophy in male rats through modulation of miR-377, let-7 b, autophagy, and fibrotic signaling pathways

Khamis

Alsemeh

Abdullah

2022

Sci Rep

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Hyperthyroidism is associated with cardiac hypertrophy, fibrosis, and increased risk of cardiovascular mortality. Sacubitril/valsartan (LCZ696) is a new combined drug that has shown promise for the treatment of hyperthyroidism-associated heart failure; however, the underlying molecular mechanisms, including the contributions of epigenetic regulation, remain unclear. The present study was designed to investigate the therapeutic efficacy of LCZ696 and the potential contributions of microRNA regulation in a rat model of hyperthyroidism-induced cardiac hypertrophy. Cardiac hypertrophy was induced by intraperitoneal administration of levothyroxine. Sixty adult male Wistar rats were randomly allocated to four equal groups (15 rats each): control, cardiac hypertrophy (CH), CH + valsartan, and CH + LCZ696. Treatment with LCZ696 or valsartan significantly improved hemodynamic abnormalities, normalized serum concentrations of natriuretic peptide, fibroblast growth factor-23, and cardiac inflammatory markers compared to CH group rats. Treatment with LCZ696 or valsartan also normalized myocardial expression levels of autophagy markers, fibrotic markers, PPAR-ϒ, mir-377, and let-7b. In addition, both valsartan and LCZ696 ameliorated collagen deposition, ventricular degeneration, and various ultrastructural abnormalities induced by levothyroxine. The beneficial effects of LCZ696 were superior to those of valsartan alone. The superior efficacy of LCZ696 may be explained by the stronger modulation of miR-377 and let-7b.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Sacubitril/valsartan (LCZ696) ameliorates hyperthyroid-induced cardiac hypertrophy in male rats through modulation of miR-377, let-7 b, autophagy, and fibrotic signaling pathways

Khamis

Alsemeh

Abdullah

2022

Sci Rep

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“…Cardiac remodeling can flexibly adjust energy supply and improve cardiac function during short periods of myocardial ischemia and hypoxia [ 87 , 88 ]. However, long-term cardiac remodeling leads to cardiac cell death [ 89 , 90 ], promoting the development of DC and ultimately developing heart failure (HF) [ 91 ].…”

Section: The Role Of Plin5 In Lipid Metabolism and DCmentioning

confidence: 99%

Plin5, a New Target in Diabetic Cardiomyopathy

Cui

Wang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Abnormal lipid accumulation is commonly observed in diabetic cardiomyopathy (DC), which can create a lipotoxic microenvironment and damage cardiomyocytes. Lipid toxicity is an important pathogenic factor due to abnormal lipid accumulation in DC. As a lipid droplet (LD) decomposition barrier, Plin5 can protect LDs from lipase decomposition and regulate lipid metabolism, which is involved in the occurrence and development of cardiovascular diseases. In recent years, studies have shown that Plin5 expression is involved in the pathogenesis of DC lipid toxicity, such as oxidative stress, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and insulin resistance (IR) and has become a key target of DC research. Therefore, understanding the relationship between Plin5 and DC progression as well as the mechanism of this process is crucial for developing new therapeutic approaches and exploring new therapeutic targets. This review is aimed at exploring the latest findings and roles of Plin5 in lipid metabolism and DC-related pathogenesis, to explore possible clinical intervention approaches.

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“…Myocardial remodeling refers to the pathological changes such as myocardial hypertrophy, myocardial apoptosis, and interstitial fibrosis induced by various pathological stimuli such as inflammation, oxidative stress, ischemia-reperfusion, and mechanical tension in the heart ( Huang et al, 2020 ). Additionally, progressive damage to mitochondrial function, imbalance of energy homeostasis, and alteration of cardiac metabolism are important characteristics of cardiac remodeling ( Sekaran et al, 2017 ; Ding et al, 2020 ).…”

Section: The Critical Role Of Endoplasmic Reticulum-mitochondria Contacts In Remodeling and Cardiovascular Remodeling-associated Diseasesmentioning

confidence: 99%

Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases

Wang

Zhang

Wen

et al. 2021

Front. Cell Dev. Biol.

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Cardiovascular remodeling occurs in cardiomyocytes, collagen meshes, and vascular beds in the progress of cardiac insufficiency caused by a variety of cardiac diseases such as chronic ischemic heart disease, chronic overload heart disease, myocarditis, and myocardial infarction. The morphological changes that occur as a result of remodeling are the critical pathological basis for the occurrence and development of serious diseases and also determine morbidity and mortality. Therefore, the inhibition of remodeling is an important approach to prevent and treat heart failure and other related diseases. The endoplasmic reticulum (ER) and mitochondria are tightly linked by ER-mitochondria contacts (ERMCs). ERMCs play a vital role in different signaling pathways and provide a satisfactory structural platform for the ER and mitochondria to interact and maintain the normal function of cells, mainly by involving various cellular life processes such as lipid metabolism, calcium homeostasis, mitochondrial function, ER stress, and autophagy. Studies have shown that abnormal ERMCs may promote the occurrence and development of remodeling and participate in the formation of a variety of cardiovascular remodeling-associated diseases. This review focuses on the structure and function of the ERMCs, and the potential mechanism of ERMCs involved in cardiovascular remodeling, indicating that ERMCs may be a potential target for new therapeutic strategies against cardiovascular remodeling-induced diseases.

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Research Progress on the Interaction Between Autophagy and Energy Homeostasis in Cardiac Remodeling

Cited by 11 publications

References 97 publications

Sacubitril/valsartan (LCZ696) ameliorates hyperthyroid-induced cardiac hypertrophy in male rats through modulation of miR-377, let-7 b, autophagy, and fibrotic signaling pathways

Sacubitril/valsartan (LCZ696) ameliorates hyperthyroid-induced cardiac hypertrophy in male rats through modulation of miR-377, let-7 b, autophagy, and fibrotic signaling pathways

Plin5, a New Target in Diabetic Cardiomyopathy

Endoplasmic Reticulum-Mitochondria Contacts: A Potential Therapy Target for Cardiovascular Remodeling-Associated Diseases

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