OTUD1 promotes pathological cardiac remodeling and heart failure by targeting STAT3 in cardiomyocytes

Wang, Mengyang; Han, Xue; Yu, Tianxiang; Luo, Wei; Zou, Chunpeng; Liu, Xiuyun; Li, Gao; Wu, Gaojun; Wang, Yi; Liang, Guang

doi:10.7150/thno.83340

Cited by 19 publications

(3 citation statements)

References 47 publications

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“…This study further elucidated that OTUD1 bound to the SH2 domain of STAT3 through its cysteine site at position 320, thereby exerting the effect of deubiquitination (Ref. 60 ).…”

Section: Role Of Deubiquitinases In Cardiac Diseasementioning

confidence: 80%

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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“…This study further elucidated that OTUD1 bound to the SH2 domain of STAT3 through its cysteine site at position 320, thereby exerting the effect of deubiquitination (Ref. 60 ).…”

Section: Role Of Deubiquitinases In Cardiac Diseasementioning

confidence: 80%

The role of deubiquitinases in cardiac disease

Zhan,

Yang,

et al. 2024

Expert Rev. Mol. Med.

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“…The infusion of Ang II is frequently utilized as an in vivo model to induce myocardial hypertrophy, inflammation, and fibrosis in mice [ 32 , 55 ]. Pressure overload induced by TAC is the prevailing mouse model for stimulating hypertrophy and heart failure [ 56 , 57 ]. According to reports, CaMKIIδ has the ability to trigger chronic inflammation in mouse heart tissue when stimulated with TAC and Ang II.…”

Section: Discussionmentioning

confidence: 99%

Sweroside alleviates pressure overload-induced heart failure through targeting CaMKⅡδ to inhibit ROS-mediated NF-κB/NLRP3 in cardiomyocytes

Wang,

Yu,

Gao

et al. 2024

Redox Biology

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“…Primary cardiomyocytes were separated according to a previous study (28). Neonatal mice (Jiangxi Zhonghong Boyuan Biotechnology Co., Ltd.) were killed, and heart tissues were extracted, washed with phosphate-buffered saline (PBS), and detached with the cocktail of tyrisin and collagenase.…”

Section: Culture Of Primary Cardiomyocytesmentioning

confidence: 99%

Cebpd Regulates Oxidative Stress and Inflammatory Responses in Hypertensive Cardiac Remodeling

Zhao,

Hu,

Zhang

et al. 2023

Shock

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Hypertension seems to inevitably cause cardiac remodeling, increasing the mortality of patients. This study aimed to explore the molecular mechanism of CCAAT enhancer binding protein delta (CEBPD)-mediated oxidative stress and inflammation in hypertensive cardiac remodeling. The hypertensive murine model was established through angiotensin-II (Ang II) injection and hypertensive mice underwent overexpressed CEBPD vector injection, cardiac function evaluation and observation of histological changes. The cell model was established by Ang II treatment and transfected with overexpressed CEBPD vector. Cell viability and surface area, oxidative stress [reactive oxygen species (ROS)/superoxide dismutase (SOD)/ superoxide dismutase (LDH)/MDA) were assessed and inflammatory factors (TNF-α/IL-1β/IL-6/IL-10) were determined both in vivo and in vitro. The levels of CEBPD, miR-96-5p, inositol 1,4,5-trisphosphate receptor 1 (IP3R), natriuretic peptide B, and natriuretic peptide A, collagen I, and collagen III in tissues and cells were determined. The binding relationships of CEBPD/miR-96-5p/IP3R 3’UTR were validated. CEBPD was reduced in cardiac tissue of hypertensive mice and CEBPD upregulation improved cardiac function and attenuated fibrosis and hypertrophy, along with reductions of ROS/LDH/MDA/TNF-α/IL-1β/IL-6 and increases in SOD/IL-10. CEBPD enriched on the miR-96-5p promoter to promote miR-96-5p expression, while CEBPD and miR-96-5p negatively regulated IP3R. miR-96-5p silencing/IP3R overexpression reversed the alleviative role of CEBPD overexpression in hypertensive mice. In summary, CEBPD promoted miR-96-5p to negatively regulate IP3R expression to inhibit oxidative stress and inflammation, thereby alleviating hypertensive cardiac remodeling.

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OTUD1 promotes pathological cardiac remodeling and heart failure by targeting STAT3 in cardiomyocytes

Cited by 19 publications

References 47 publications

The role of deubiquitinases in cardiac disease

The role of deubiquitinases in cardiac disease

Sweroside alleviates pressure overload-induced heart failure through targeting CaMKⅡδ to inhibit ROS-mediated NF-κB/NLRP3 in cardiomyocytes

Cebpd Regulates Oxidative Stress and Inflammatory Responses in Hypertensive Cardiac Remodeling

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