Co‑expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia‑reperfusion injury by promoting angiogenesis and inhibiting oxidative stress

Huang, Shujie; Chen, Meixian; Yu, Hanjie; Lin, Kaiyang; Guo, Yujin; Zhu, Pengli

doi:10.3892/mmr.2020.11805

Cited by 4 publications

(2 citation statements)

References 39 publications

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“…Ligation of left anterior descending for 2 h was performed to induce MIRI. The ischemia of the anterior wall of left ventricular was confirmed by the ST-segment elevation on the electrocardiogram [ 23 ]. The average phenotype/infarct size of MIRI animal had been confirmed with our preliminary experiment.…”

Section: Methodsmentioning

confidence: 99%

Uric acid promotes myocardial infarction injury via activating pyrin domain-containing 3 inflammasome and reactive oxygen species/transient receptor potential melastatin 2/Ca2+pathway

Dai

Wang

et al. 2023

BMC Cardiovasc Disord

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Cardiomyocytes injury has been considered as a key contributor for myocardial infarction (MI). Uric acid (UA) can induce cardiomyocytes injury, which is closely related to NLRP3 activation and inflammatory factor generation. However, the mechanism how UA modulates cardiomyocytes remains elusive. Western blotting and qRT-PCR were applied for measuring protein and mRNA expression, respectively. ROS production and Ca2+ influx were measured by flow cytometry. Patch clamp technique was used for measuring transient receptor potential melastatin 2 (TRPM2) channel. Ligation of left anterior descending for 2 h was performed to induce MI animal model. The rats were treated by different concentration of uric acid. The artery tissues were stained by HE and collected for measurement of NLRP3 and inflammatory factors. Supplementation of UA significantly promoted apoptosis, and augmented the expression of intercellular adhesion molecule-1, chemoattractant protein-1, vascular cell adhesion molecule-1, and NLRP3 inflammasome. Knockdown of NLRP3 reversed the influence of UA on MI by decreasing collagen deposition, fibrotic area, apoptosis. The expression of NLRP3 inflammasome increased markedly after treatment of UA. UA activated ROS/TRPM2/Ca2+ pathway through targeting NLRP3. UA activated NLRP3 inflammasome and augments inflammatory factor production, which in turn exacerbates cardiomyocytes injury. Knockdown of NLRP3 reversed the influence of UA on apoptosis and cell cycle. UA may promote cardiomyocytes injury through activating NLRP3 inflammasome and ROS/TRPM2 channel/Ca2+ pathway.

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Section: Methodsmentioning

confidence: 99%

Uric acid promotes myocardial infarction injury via activating pyrin domain-containing 3 inflammasome and reactive oxygen species/transient receptor potential melastatin 2/Ca2+pathway

Dai

Wang

et al. 2023

BMC Cardiovasc Disord

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“…More severely, the endothelial cell damage caused by hydrogen peroxide exceeding 126 μ M is fatal [ 75 , 76 ]. Similar to this view, the joint expression of hTK1 and hTIMP1 genes can weaken oxidative stress and contribute to the formation of new blood vessels [ 77 ].…”

Section: The Mechanism Of Angiogenesis After Myocardial Infarctionmentioning

confidence: 97%

Natural Herbal Medicine as a Treatment Strategy for Myocardial Infarction through the Regulation of Angiogenesis

Zhang

Song

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Aim of Study. Myocardial infarction is the number one cause of death worldwide. Existing treatment methods such as drugs and surgery cannot completely restore the structure and function of the ischemic heart. In recent years, therapeutic angiogenesis has received gradually increasing attention due to its fundamental therapeutic advantages of improving microcirculation and restoring blood supply in ischemic areas. This article mainly reviewed the mechanism and effect of angiogenesis-promoting herbs. Methods. We conducted a literature search on the bioactive components of medicinal plants and their effects on angiogenesis after MI. We searched for articles in Web of Science, MEDLINE, PubMed, Scopus, Google Scholar, and China National Knowledge Infrastructure databases before April 2021. Results. In this article, we summarized the mechanisms by which copper ions, microRNA, Akt1, inflammation, oxidative stress, mitochondria, and pericytes are involved in angiogenesis after myocardial infarction. In addition, we reviewed the angiogenic effects of natural herbal medicines such as Salvia miltiorrhiza Bunge Bunge, Carthamus tinctorius L., Pueraria lobata, Astragalus, Panax ginseng C.A. Mey., Panax notoginseng (Burkill) F.H. Chen, Cinnamomum cassia (L.) J. Presl, Rehmannia glutinosa (Gaertn.) DC., Leonurus japonicus Houtt, Scutellaria baicalensis Georgi., and Geum macrophyllum Willd. Conclusions. Some herbs have the effect of promoting angiogenesis. In the future, natural proangiogenic drugs may become candidates for the treatment of cardiovascular diseases.

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Kallistatin attenuates inflammatory response in rheumatoid arthritis via the NF-κB signaling pathway

Wang

Huang

Gao

et al. 2023

European Journal of Pharmacology

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Co‑expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia‑reperfusion injury by promoting angiogenesis and inhibiting oxidative stress

Cited by 4 publications

References 39 publications

Uric acid promotes myocardial infarction injury via activating pyrin domain-containing 3 inflammasome and reactive oxygen species/transient receptor potential melastatin 2/Ca2+pathway

Uric acid promotes myocardial infarction injury via activating pyrin domain-containing 3 inflammasome and reactive oxygen species/transient receptor potential melastatin 2/Ca2+pathway

Natural Herbal Medicine as a Treatment Strategy for Myocardial Infarction through the Regulation of Angiogenesis

Kallistatin attenuates inflammatory response in rheumatoid arthritis via the NF-κB signaling pathway

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