ArticleExperimental & molecular medicine2022
CU06-1004 enhances vascular integrity and improves cardiac remodeling by suppressing edema and inflammation in myocardial ischemia-reperfusion injury.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Nanocarrier-Based Therapeutic Strategies in Myocardial Ischemia-Reperfusion Injury: A Systematic Review of Preclinical Evidence.Biomedicines · 2026Review
- Myocardial Ischemia-Reperfusion Injury-Mechanistic Insights and Novel Therapeutics.International journal of molecular sciences · 2026Review
- Iron-dependent ferroptosis in cardiac microvascular endothelial cells: a key link between dysregulated iron homeostasis and microcirculatory injury during myocardial ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Review
- CU104, a novel barrier function enhancer, improves colitis via modulation of barrier function and immune cell recruitment.Frontiers in immunology · 2026Article
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
- Vascularized and Perfusable Human Heart-on-a-Chip Model Recapitulates Aspects of Myocardial Ischemia and Enables Analysis of Nanomedicine Delivery.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Network pharmacology-based prediction and molecular docking-based strategy to investigate the potential mechanism of Leonurus japonicus Houtt. Against myocardial ischemia reperfusion injury.Journal of cardiothoracic surgery · 2025Article
- Endothelial FOSL1 drives angiotensin II-induced myocardial injury via AT1R-upregulated MYH9.Acta pharmacologica Sinica · 2025Article
- ARNT-dependent HIF-2α signaling protects cardiac microvascular barrier integrity and heart function post-myocardial infarction.Communications biology · 2025Article
- Cardioprotective strategies in myocardial ischemia-reperfusion injury: Implications for improving clinical translation.Journal of molecular and cellular cardiology plus · 2025Review
- CU06-1004 inhibits the progression of chronic colitis and colitis-associated colorectal cancer by suppressing inflammation.Frontiers in pharmacology · 2025Article
- Role of NLRP3 Inflammasome in Heart Failure Patients Undergoing Cardiac Surgery as a Potential Determinant of Postoperative Atrial Fibrillation and Remodeling: Is SGLT2 Cotransporter Inhibition an Alternative for Cardioprotection?Antioxidants (Basel, Switzerland) · 2024Review
- Mechanisms of the septic heart: From inflammatory response to myocardial edema.Journal of molecular and cellular cardiology · 2024Review
- Article
- Immuno-inflammatory pathogenesis in ischemic heart disease: perception and knowledge for neutrophil recruitment.Frontiers in immunology · 2024Review
- Report from the 2023 workshop on endothelial permeability, edema and inflammation.Nature cardiovascular research · 2023Article
- Are There Hopeful Therapeutic Strategies to Regenerate the Infarcted Hearts?Korean circulation journal · 2023Review
- Review
- Efficacy of CU06-1004 via regulation of inflammation and endothelial permeability in LPS-induced acute lung injury.Journal of inflammation (London, England) · 2023Article
- CU06-1004 as a promising strategy to improve anti-cancer drug efficacy by preventing vascular leaky syndrome.Frontiers in pharmacology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia-reperfusion (I/R) injury accelerates the cardiomyocytes (CMs) death by oxidative stress, and thereby deteriorates cardiac function. There has been a paradigm shift in the therapeutic perspective more towards the prevention or amelioration of damage caused by reperfusion. Cardiac microvascular endothelial cells (CMECs) are more vulnerable to reperfusion injury and play the crucial roles more than CMs in the pathological process of early I/R injury. In this study, we investigate that CU06-1004, as a vascular leakage blocker, can improve cardiac function by inhibiting CMEC's hyperpermeability and subsequently reducing the neutrophil's plugging and infiltration in infarcted hearts. CU06-1004 was delivered intravenously 5 min before reperfusion and the rats were randomly divided into three groups: (1) vehicle, (2) low-CU06-1004 (1 mg/kg, twice at 24 h intervals), and (3) high-CU06-1004 (5 mg/kg, once before reperfusion). CU06-1004 treatment reduced necrotic size and cardiac edema by enhancing vascular integrity, as demonstrated by the presence of intact junction proteins on CMECs and surrounding pericytes in early I/R injury. It also decreased the expression of vascular cell adhesion molecule 1 (VCAM-1) on CMECs, resulting in reduced infiltration of neutrophils and macrophages. Echocardiography showed that the CU06-1004 treatment significantly improved cardiac function compared with the vehicle group. Interestingly, single high-dose treatment with CU06-1004 provided a greater functional improvement than repetitive low-dose treatment until 8 weeks post I/R. These findings demonstrate that CU06-1004 enhances vascular integrity and improves cardiac function by preventing lethal myocardial I/R injury. It can provide a promising therapeutic option, as potential adjunctive therapy to current reperfusion strategies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.