E3 ubiquitin ligase mind bomb 1 overexpression reduces apoptosis and inflammation of cardiac microvascular endothelial cells in coronary microvascular dysfunction

Qin, Xuda; Shan, Yingguang; Gao, Jinghong; Li, Fengxiang; Guo, Yu-xi

doi:10.1016/j.cellsig.2021.110223

Cited by 10 publications

(4 citation statements)

References 24 publications

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“…Seo et al [71] found that MIB1 was responsible for the proteasomal degradation-dependent regulation of α-actinin 3 in skeletal muscle maintenance. Recently, Qin et al reported that MIB1 overexpression relieved apoptosis and inflammation of cardiac microvascular endothelial cells during coronary microvascular dysfunction by targeting the ASK1/p38 pathway [72]. In agreement with the hypothesis, lncZFAS1 overexpression directly interfered with mir590-3p to inhibit TXNIP the MIB1 E3 ubiquitin ligase/NLRP3 pathway [6].…”

Section: Interaction Between Lncrna Zfas1 and Mirnas In Pd Neuroimmun...mentioning

confidence: 61%

LncZFAS1 Inhibit MPP+-Induced Neuroinflammation Through TXNIP/MIB1 E3 Ubiquitin Ligase/NLRP3 Axis

2022

Journal of Cellular Immunology

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Neuroinflammation is associated with the occurrence and progression of Parkinson's disease (PD). Nucleotide-binding domain-like receptor protein-3 (NLRP3) is closely related to pyroptosis in PD-related cells and animal models, such as microglia and SH-SY5Y cells. The novel lncRNA ZFAS1 (LncZFAS1) regulates a variety of signaling pathways and participates in the inflammatory response in various diseases. However, their role in PD remains unclear. Our research found LncZFAS1 overexpression directly interfered with mir590-3p to inhibit thioredoxin-interacting protein (TXNIP) the Mindbomb 1 (MIB1) E3 ubiquitin ligase/NLRP3 pathway, which might reveal a new research approach to the mechanism of PD.

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Section: Interaction Between Lncrna Zfas1 and Mirnas In Pd Neuroimmun...mentioning

confidence: 61%

LncZFAS1 Inhibit MPP+-Induced Neuroinflammation Through TXNIP/MIB1 E3 Ubiquitin Ligase/NLRP3 Axis

2022

Journal of Cellular Immunology

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“…41 Qin et al identified ASK1 as a substrate of E3 ubiquitin ligase MIB1. 42 They found that overexpression of MIB1 alleviated homocysteine-induced apoptosis and inflammation in cardiac microvascular ECs by promoting ASK1 ubiquitination and degradation. 42 Qian et al 43 demonstrated that the E3 ubiquitin ligase Smurf2 enhanced the ubiquitination and degradation of PARP1, a substrate of caspase 3, thereby alleviating oxidative stress-induced HUVEC apoptosis.…”

Section: The Role and Mechanism Of E3 Ubiquitin Ligase In Regulating ...mentioning

confidence: 99%

E3 Ubiquitin Ligases in Endothelial Dysfunction and Vascular Diseases: Roles and Potential Therapies

Wang

Zhan

Wang

et al. 2023

Journal of Cardiovascular Pharmacology

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Ubiquitin E3 ligases are a structurally conserved family of enzymes that exert a variety of regulatory functions in immunity, cell death, and tumorigenesis through the ubiquitination of target proteins. Emerging evidence has shown that E3 ubiquitin ligases play crucial roles in the pathogenesis of endothelial dysfunction and related vascular diseases. Here, we reviewed the new findings of E3 ubiquitin ligases in regulating endothelial dysfunction, including endothelial junctions and vascular integrity, endothelial activation, and endothelial apoptosis. The critical role and potential mechanism of E3 ubiquitin ligases in vascular diseases, such as atherosclerosis, diabetes, hypertension, pulmonary hypertension, and acute lung injury, were summarized. Finally, the clinical significance and potential therapeutic strategies associated with the regulation of E3 ubiquitin ligases were also proposed.

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“…Another study found that increased release of inflammatory factors leads to impaired vascular endothelial barrier function after coronary artery occlusion ( 34 , 35 ). Qin et al ( 36 ) found that the expression of inflammation-related factors TNF-α and IL-1β was increased in an in vitro and in vivo model of CMVD. In conclusion, inflammatory response plays an important role in the pathogenesis of CMVD.…”

Section: Relationship Between Inflammatory Response and Cmvdmentioning

confidence: 99%

Inflammation and coronary microvascular disease: relationship, mechanism and treatment

Guo,

Yang,

Song

et al. 2024

Front. Cardiovasc. Med.

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Coronary microvascular disease (CMVD) is common in patients with cardiovascular risk factors and is linked to an elevated risk of adverse cardiovascular events. Although modern medicine has made significant strides in researching CMVD, we still lack a comprehensive understanding of its pathophysiological mechanisms due to its complex and somewhat cryptic etiology. This greatly impedes the clinical diagnosis and treatment of CMVD. The primary pathological mechanisms of CMVD are structural abnormalities and/or dysfunction of coronary microvascular endothelial cells. The development of CMVD may also involve a variety of inflammatory factors through the endothelial cell injury pathway. This paper first reviews the correlation between the inflammatory response and CMVD, then summarizes the possible mechanisms of inflammatory response in CMVD, and finally categorizes the drugs used to treat CMVD based on their effect on the inflammatory response. We hope that this paper draws attention to CMVD and provides novel ideas for potential therapeutic strategies based on the inflammatory response.

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E3 ubiquitin ligase mind bomb 1 overexpression reduces apoptosis and inflammation of cardiac microvascular endothelial cells in coronary microvascular dysfunction

Cited by 10 publications

References 24 publications

LncZFAS1 Inhibit MPP+-Induced Neuroinflammation Through TXNIP/MIB1 E3 Ubiquitin Ligase/NLRP3 Axis

LncZFAS1 Inhibit MPP+-Induced Neuroinflammation Through TXNIP/MIB1 E3 Ubiquitin Ligase/NLRP3 Axis

E3 Ubiquitin Ligases in Endothelial Dysfunction and Vascular Diseases: Roles and Potential Therapies

Inflammation and coronary microvascular disease: relationship, mechanism and treatment

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