Ubiquitin Carboxyl-Terminal Hydrolase L1 of Cardiomyocytes Promotes Macroautophagy and Proteostasis and Protects Against Post-myocardial Infarction Cardiac Remodeling and Heart Failure

Wu, Penglong; Li, Yifan; Cai, Mingqi; Ye, Bo; Geng, Bingchuan; Li, Faqian; Zhu, Hua; Liu, Jinbao; Wang, Xuejun

doi:10.3389/fcvm.2022.866901

Cited by 6 publications

(5 citation statements)

References 33 publications

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“…Azad et al 13 demonstrated that prolonged hypoxia can induce autophagic cell death, which may represent a potential target for preventing cell death. Wu et al 14 reported that autophagy induction following cardiac hypoxia or ischemic injury may play a pathogenic role in heart disease. In view of the controversy of autophagy, the fact is that apoptosis and autophagy interact and play a key role in regulating cell survival during HF.…”

Section: Introductionmentioning

confidence: 99%

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Lian,

Tong,

Zhu

et al. 2023

Clin Exp Pharma Physio

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Preventing or treating heart failure (HF) by blocking cardiomyocyte apoptosis is an effective strategy that improves survival and reduces ventricular remodelling and dysfunction in the chronic stage. Autophagy is a mechanism that degrades intracellular components and compensates for energy deficiency, which is commonly observed in cardiomyocytes of failed hearts. Cardiomyocytes activated by doxorubicin (DOX) exhibit strong autophagy. This study aims to investigate the potential protective effect of ligustrazine and its derivative liguzinediol on regulating DOX‐induced cardiomyocyte apoptosis and explore the use of the embryonic rat heart‐derived myoblast cell line H9C2 for identifying novel treatments for HF. The results indicated that it has been demonstrated to reverse myocardial infarction remodelling in failed hearts by promoting autophagy in salvaged cardiomyocytes and anti‐apoptosis of cardiomyocytes in granulation tissue. Our study suggests that ligustrazine and liguzinediol can be a promising agents and autophagy is potential pathway in the management of HF.

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Section: Introductionmentioning

confidence: 99%

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Lian,

Tong,

Zhu

et al. 2023

Clin Exp Pharma Physio

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“… Geng et al (2022) compared the ischemic heart injury group with the control group and found the overexpression of UCHL1 has a protective effect on myocardial injury after myocardial infarction. Upregulation of UCHL1 can prevent cardiac remodeling and dysfunction after myocardial infarction by supporting autophagy flow and protein homeostasis ( Wu et al, 2022 ). For the GPC6 gene, a previous study found that compared to patients with heart failure after myocardial infarction, patients without heart failure had significantly lower glypican-6, suggesting that GPC6 may be a protective gene for heart failure after myocardial infarction ( Ozturk et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Predicting protective gene biomarker of acute coronary syndrome by the circRNA-associated competitive endogenous RNA regulatory network

Zhang

Merkus²,

Zhang³

et al. 2022

Front. Genet.

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Background: The mortality and disability rates of acute coronary syndrome (ACS) are quite high. Circular RNA (circRNA) is a competitive endogenous RNA (ceRNA) that plays an important role in the pathophysiology of ACS. Our goal is to screen circRNA-associated ceRNA networks for biomarker genes that are conducive to the diagnosis or exclusion of ACS, and better understand the pathology of the disease through the analysis of immune cells.Materials and methods: RNA expression profiles for circRNAs (GSE197137), miRNAs (GSE31568), and mRNAs (GSE95368) were obtained from the GEO database, and differentially expressed RNAs (DEcircRNAs, DEmiRNAs, and DEmRNAs) were identified. The circRNA-miRNA and miRNA-mRNA regulatory links were retrieved from the CircInteractome database and TargetScan databases, respectively. As a final step, a regulatory network has been designed for ceRNA. On the basis of the ceRNA network, hub mRNAs were verified by quantitative RT-PCR. Hub genes were validated using a third independent mRNA database GSE60993, and ROC curves were used to evaluate their diagnostic values. The correlation between hub genes and immune cells associated with ACS was then analyzed using single sample gene set enrichment analysis (ssGSEA).Results: A total of 17 DEcircRNAs, 229 DEmiRNAs, and 27 DEmRNAs were found, as well as 52 circRNA-miRNA pairings and 10 miRNA-mRNA pairings predicted. The ceRNA regulatory network (circRNA-miRNA-mRNA) was constructed, which included 2 circRNA (hsa_circ_0082319 and hsa_circ_0005654), 4 miRNA (hsa-miR-583, hsa-miR-661, hsa-miR-671-5p, hsa-miR-578), and 5 mRNA (XPNPEP1, UCHL1, DBNL, GPC6, and RAD51). The qRT-PCR analysis result showed that the XPNPEP1, UCHL1, GPC6 and RAD51 genes had a significantly decreased expression in ACS patients. Based on ROC curve analysis, we found that XPNPEP1 has important significance in preventing ACS occurrence and excluding ACS diagnosis. ACS immune infiltration analysis revealed significant correlations between the other 3 hub genes (UCHL1, GPC6, RAD51) and the immune cells (Eosinophils, T folliculars, Type 2 T helper cells, and Imumature dendritic cells).Conclusion: Our study constructed a circRNA-related ceRNA network in ACS. The XPNPEP1 gene could be a protective gene biomarker for ACS. The UCHL1, GPC6 and RAD51 genes were significantly correlated with immune cells in ACS.

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“…No abnormalities were observed in the cardiac development of UCHL1-specific knockout mice before 14 weeks of age (Ref. 99 ) ( Fig. 2 ).…”

Section: Role Of Deubiquitinases In Cardiac Diseasementioning

confidence: 93%

The role of deubiquitinases in cardiac disease

Zhan,

Yang,

et al. 2024

Expert Rev. Mol. Med.

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Deubiquitinases are a group of proteins that identify and digest monoubiquitin chains or polyubiquitin chains attached to substrate proteins, preventing the substrate protein from being degraded by the ubiquitin-proteasome system. Deubiquitinases regulate cellular autophagy, metabolism and oxidative stress by acting on different substrate proteins. Recent studies have revealed that deubiquitinases act as a critical regulator in various cardiac diseases, and control the onset and progression of cardiac disease through a board range of mechanism. This review summarizes the function of different deubiquitinases in cardiac disease, including cardiac hypertrophy, myocardial infarction and diabetes mellitus-related cardiac disease. Besides, this review briefly recapitulates the role of deubiquitinases modulators in cardiac disease, providing the potential therapeutic targets in the future.

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Ubiquitin Carboxyl-Terminal Hydrolase L1 of Cardiomyocytes Promotes Macroautophagy and Proteostasis and Protects Against Post-myocardial Infarction Cardiac Remodeling and Heart Failure

Cited by 6 publications

References 33 publications

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Predicting protective gene biomarker of acute coronary syndrome by the circRNA-associated competitive endogenous RNA regulatory network

The role of deubiquitinases in cardiac disease

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