Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b

Liu, Qi; Chen, Liyang; Xia, Liang; Cao, Yuqing; Zhu, Xinyue; Wang, Siqi; Li, Jin; Gao, Juan; Xiao, Junjie

doi:10.1016/j.jshs.2021.06.002

Cited by 32 publications

(19 citation statements)

References 43 publications

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“…At the same time, it is also a risk factor for atherosclerosis in elderly patients and a predictor of poor prognosis for elderly patients with percutaneous coronary intervention (PCI). Studies have extensively shown that sarcopenia may be involved in the development and progression of CHD ( 3 , 30 , 52 ). The study included a total of 475 elderly patients with coronary artery disease who underwent successful PCI to assess sarcopenia by measuring the cross-sectional area of skeletal muscle at the first lumbar vertebra (L1) and exploring the impact of low skeletal muscle mass on the prognosis of patients with coronary artery disease who underwent successful PCI.…”

Section: Sarcopenia and Cvdsmentioning

confidence: 99%

“…Physical exercise is an economical, safe, and effective intervention for both CVDs and sarcopenia. Physical exercise methods include active and passive exercise and aerobic and resistance exercise, increasing muscle mass and strength, improving exercise and balance ability, and reducing falls and fractures ( 52 , 85 – 88 ). Aerobic exercise can be carried out with simple equipment such as swimming, jogging, and push-ups or with the aid of elastic bands.…”

Section: Joint Intervention Of Sarcopenia and Cvdsmentioning

confidence: 99%

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Relationship Between Sarcopenia and Cardiovascular Diseases in the Elderly: An Overview

Zhang

et al. 2021

Front. Cardiovasc. Med.

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With the advent of population aging, aging-related diseases have become a challenge for governments worldwide. Sarcopenia has defined as a clinical syndrome associated with age-related loss such as skeletal muscle mass, strength, function, and physical performance. It is commonly seen in elderly patients with chronic diseases. Changes in lean mass are common critical determinants in the pathophysiology and progression of cardiovascular diseases (CVDs). Sarcopenia may be one of the most important causes of poor physical function and decreased cardiopulmonary function in elderly patients with CVDs. Sarcopenia may induce CVDs through common pathogenic pathways such as malnutrition, physical inactivity, insulin resistance, inflammation; these mechanisms interact. In this study, we aimed to investigate the relationship between sarcopenia and CVDs in the elderly. Further research is urgently needed to understand better the relationship, pathophysiology, clinical presentation, diagnostic criteria, and mechanisms of sarcopenia and CVDs, which may shed light on potential interventions to improve clinical outcomes and provide greater insight into the disorders above.

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Section: Sarcopenia and Cvdsmentioning

confidence: 99%

Section: Joint Intervention Of Sarcopenia and Cvdsmentioning

confidence: 99%

Relationship Between Sarcopenia and Cardiovascular Diseases in the Elderly: An Overview

Zhang

et al. 2021

Front. Cardiovasc. Med.

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“… 5 miR-29b has been showed to promote many types of muscle atrophy including heart failure-induced muscle wasting via regulating target genes IGF-1, PI3K, and YY1. 50 , 51 Peroxisome proliferator activated receptor gamma (PPARγ) was found to inhibit AngII-induced muscle atrophy and improve muscle function by targeting and downregulating miR-29b; 51 , 52 similarly, inhibition of miR-29b by the CRISPR-Cas9 editing system significantly attenuated AngII-induced muscle atrophy in vivo . 53 It is noteworthy that several muscle-specific miRNAs, including miR-1, miR-133a, miR-133b, miR-208a, and miR-208b, have been found to be involved in the regulation of both cardiac and skeletal muscle functions.…”

Section: Ncrnas In Muscle Atrophy Induced By Heart Failurementioning

confidence: 99%

Non-coding RNA basis of muscle atrophy

Liu

Deng

Qiu

et al. 2021

Molecular Therapy - Nucleic Acids

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Muscle atrophy is a common complication of many chronic diseases including heart failure, cancer cachexia, aging, etc. Unhealthy habits and usage of hormones such as dexamethasone can also lead to muscle atrophy. However, the underlying mechanisms of muscle atrophy are not completely understood. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), play vital roles in muscle atrophy. This review mainly discusses the regulation of ncRNAs in muscle atrophy induced by various factors such as heart failure, cancer cachexia, aging, chronic obstructive pulmonary disease (COPD), peripheral nerve injury (PNI), chronic kidney disease (CKD), unhealthy habits, and usage of hormones; highlights the findings of ncRNAs as common regulators in multiple types of muscle atrophy; and summarizes current therapies and underlying mechanisms for muscle atrophy. This review will deepen the understanding of skeletal muscle biology and provide new strategies and insights into gene therapy for muscle atrophy.

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“…Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining Tissue fractions from each group were analyzed using a TUNEL assay (ab66108, Abcam, Cambridge, UK), as described previously 21 . Images were captured using a uorescence microscope at 400× magni cation.…”

Section: Propidium Iodide (Pi) Stainingmentioning

confidence: 99%

Transmembrane p24 Trafficking Protein 2 Regulates Inflammation Through the TLR4/NF-κB Signaling Pathway in Lung Adenocarcinoma

Feng

Cheng

Feng

et al. 2021

Preprint

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Background: To investigate the role of transmembrane p24 trafficking protein 2 (TMED2) in lung adenocarcinoma (LUAD) and determine whether TMED2 knockdown could inhibit LUAD in vitro and in vivo.Methods: TIMER2.0, Kaplan-Meier plotter, gene set enrichment analysis (GSEA), Target Gene, and pan-cancer systems were used to predict the potential function of TMED2. Western blotting and immunohistochemistry were performed to analyze TMED2 expression in different tissues or cell lines. The proliferation, development, and apoptosis of LUAD were observed using a lentivirus-mediated TMED2 knockdown. Bioinformatics and western blot analysis of TMED2 against inflammation via the TLR4/NF-κB signaling pathway were conducted. Results: TMED2 expression in LUAD tumor tissues was higher than that in normal tissues and positively correlated with poor survival in lung cancer and negatively correlated with apoptosis in LUAD. The expression of TMED2 was higher in tumors or HCC827 cells. TMED2 knockdown inhibited LUAD development in vitro and in vivo and increased the levels of inflammatory factors via the TLR4/NF-κB signaling pathway. TMED2 was correlated with TME, immune score, TME-associated immune cells, their target markers, and some mechanisms and pathways, as determined using the TIMER2.0, GO, and KEGG assays.Conclusions: TMED2 may regulate inflammation in LUAD through the TLR4/NF-κB signaling pathway, and enhance the proliferation, development, and prognosis of LUAD by regulating inflammation, which provide a new strategy for treating LUAD by regulating inflammation.

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Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b

Cited by 32 publications

References 43 publications

Relationship Between Sarcopenia and Cardiovascular Diseases in the Elderly: An Overview

Relationship Between Sarcopenia and Cardiovascular Diseases in the Elderly: An Overview

Non-coding RNA basis of muscle atrophy

Transmembrane p24 Trafficking Protein 2 Regulates Inflammation Through the TLR4/NF-κB Signaling Pathway in Lung Adenocarcinoma

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