Hypoxia-inducible factor-1α attenuates myocardial inflammatory injury in rats induced by coronary microembolization

Chen, Quan-Fang; Wang, Wei; Huang, Zhou; Huang, Dongling

doi:10.1590/0001-3765202020190658

Cited by 10 publications

(7 citation statements)

References 23 publications

(10 reference statements)

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“…In addition, some metabolism-related factors are also involved in the regulation of the TLR4/MyD88/NF-κB pathway as follows: HIF-1α and apolipoprotein A-I mimetic peptide 4F (4F) may attenuate myocardial injury by minimizing TLR4 upregulation in post-MI rats 228,229 ; cardiac TLR4 is preferentially upregulated by oxidized cholesterol in rats with MI 230 . Similarly, activation of the TLR4-MyD88 signaling pathway in a hyperlipidemic environment inhibits the lisinopril-mediated cardioprotective effect 231 .…”

Section: Tlr4/myd88/nf-κb-signaling Pathway In MI Innate Immune Cells...mentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

285

117

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Although the treatment of myocardial infarction (MI) has improved considerably, it is still a worldwide disease with high morbidity and high mortality. Whilst there is still a long way to go for discovering ideal treatments, therapeutic strategies committed to cardioprotection and cardiac repair following cardiac ischemia are emerging. Evidence of pathological characteristics in MI illustrates cell signaling pathways that participate in the survival, proliferation, apoptosis, autophagy of cardiomyocytes, endothelial cells, fibroblasts, monocytes, and stem cells. These signaling pathways include the key players in inflammation response, e.g., NLRP3/caspase-1 and TLR4/MyD88/NF-κB; the crucial mediators in oxidative stress and apoptosis, for instance, Notch, Hippo/YAP, RhoA/ROCK, Nrf2/HO-1, and Sonic hedgehog; the controller of myocardial fibrosis such as TGF-β/SMADs and Wnt/β-catenin; and the main regulator of angiogenesis, PI3K/Akt, MAPK, JAK/STAT, Sonic hedgehog, etc. Since signaling pathways play an important role in administering the process of MI, aiming at targeting these aberrant signaling pathways and improving the pathological manifestations in MI is indispensable and promising. Hence, drug therapy, gene therapy, protein therapy, cell therapy, and exosome therapy have been emerging and are known as novel therapies. In this review, we summarize the therapeutic strategies for MI by regulating these associated pathways, which contribute to inhibiting cardiomyocytes death, attenuating inflammation, enhancing angiogenesis, etc. so as to repair and re-functionalize damaged hearts.

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Section: Tlr4/myd88/nf-κb-signaling Pathway In MI Innate Immune Cells...mentioning

confidence: 99%

Signaling pathways and targeted therapy for myocardial infarction

Zhang

Wang

et al. 2022

Sig Transduct Target Ther

285

117

View full text Add to dashboard Cite

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“…Hypoxia-induced factor-1α (HIF-1α), a key transcription factor, is crucial in inflammatory pathways. HIF-1α attenuates myocardial inflammation and may be linked to the NLRP3 inflammasome pathway ( Chen et al, 2020 ). It also reduces inflammation via miR-380-3p/NLRP3 ( Li et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Ligand-gated ion channel P2X7 regulates hypoxia-induced factor-1α mediated pain induced by dental pulpitis in the medullary dorsal horn

Zhang

Liang

et al. 2022

Front. Mol. Neurosci.

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Dental pulpitis often induces severe pain, and the molecular immune response is remarkable in both peripheral and central nervous system. Accumulating evidence indicates that activated microglia in the medullary dorsal horn (MDH) contribute to dental pulpitis induced pain. The P2X7 receptor plays an important role in driving pain and inflammatory processes, and its downstream target hypoxia-induced factor-1α (HIF-1α) has a crucial role in maintaining inflammation. However, the relationship between P2X7 and HIF-1α in dental inflammatory pain remains unclear. This study demonstrated that the degree of inflammation in the dental pulp tissue became more severe in a time-dependent manner by establishing a rat dental pulpitis model via pulp exposure. Meanwhile, the expression of P2X7, HIF-1α, IL-1β, and IL-18 in the MDH increased most on the seventh day when the pain threshold was the lowest in the dental pulpitis model. Furthermore, lipopolysaccharides (LPS) increased P2X7-mediated HIF-1α expression in microglia. Notably, the suppression of P2X7 caused less IL-1β and IL-18 release and lower HIF-1α expression, and P2X7 antagonist Brilliant Blue G (BBG) could alleviate pain behaviors of the dental pulpitis rats. In conclusion, our results provide further evidence that P2X7 is a key molecule, which regulates HIF-1α expression and inflammation in dental pulpitis-induced pain.

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“…For example, this is achieved by limiting activity for 6 h, followed by stimulation by clamping the tail for 5 min daily for 14 days [ 170 ]. coronary microembolization [ 171 ] is the introduction of a suspension of saline microspheres in the left ventricle during 10s occlusion of the ascending aorta. reproduction of ischemic cardiomyopathy by permanent ligation of the left coronary artery in rats [ 172 ].…”

Section: Methodology Of Literature Search and Selectionmentioning

confidence: 99%

“…coronary microembolization [ 171 ] is the introduction of a suspension of saline microspheres in the left ventricle during 10s occlusion of the ascending aorta.…”

Section: Methodology Of Literature Search and Selectionmentioning

confidence: 99%