Bioderived Nanoparticles for Cardiac Repair

ACS Nano, Journal Year: 2024, Volume and Issue: 18(36), P. 24622 - 24649

Published: Aug. 26, 2024

Biobased therapy represents a promising strategy for myocardial repair. However, the limitations of using live cells, including risk immunogenicity allogeneic cells and inconsistent therapeutic efficacy autologous together with low stability, result in an unsatisfactory clinical outcomes. Therefore, cell-free strategies cardiac tissue repair have been proposed as alternative strategies. Cell-free strategies, primarily based on paracrine effects cellular therapy, demonstrated their potential to inhibit apoptosis, reduce inflammation, promote on-site cell migration proliferation, well angiogenesis, after infarction explored preclinically clinically. Among various modalities, bioderived nanoparticles, adeno-associated virus (AAV), extracellular vesicles, membrane-coated exosome-mimetic nanovesicles, emerged due improved biological function effect. The main focus this review is development existing nanoparticles fundamental working mechanisms, challenges opportunities. key processes requirements are summarized first. Various nanoparticle modalities further highlighted, advantages limitations. Finally, we discuss delivery approaches that offer pathways researchers clinicians translate into practice.

Language: Английский

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Astragaloside IV Exerts a Myocardial Protective Effect against Cardiac Hypertrophy in Rats, Partially via Activating the Nrf2/HO-1 Signaling Pathway

Oxidative Medicine and Cellular Longevity, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 16

Published: June 11, 2019

Previous evidence suggested that astragaloside IV (ASIV) had a cardioprotective effect, but the potential mechanisms were undetermined. This study is aimed at validating prevention of cardiac hypertrophy in chronic heart failure (CHF) rats and H9c2 cardiomyocytes by ASIV exploring mechanism involved. CHF rat models abdominal aortic constriction (AAC) used with aim determining protective effect rats. We proved could attenuate improving left ventricular function structure showed expression nuclear factor-erythroid 2-related factor 2 (Nrf2) its downstream gene heme oxygenase-1 (HO-1) increased high-dose intervention group. To further investigate specific ASIV, we hypothesized might prevent via activating Nrf2/HO-1 signaling pathway. established cardiomyocyte model induced angiotensin II (Ang II), which was then transfected Nrf2 shRNA, to knock down gene. found against Ang II-induced abolished shRNA transfection group, ultimately aggravating II, it possible oxidative stress may be involved this process. Our results demonstrated improved inhibited upregulating Nrf2, partially achieved stimulating pathway, suggesting have therapeutic for treatment CHF.

Language: Английский

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<p>Liraglutide attenuates cardiac remodeling and improves heart function after abdominal aortic constriction through blocking angiotensin II type 1 receptor in rats</p>

Drug Design Development and Therapy, Journal Year: 2019, Volume and Issue: Volume 13, P. 2745 - 2757

Published: Aug. 1, 2019

Angiotensin II (Ang II) is known to contribute the pathogenesis of heart failure by eliciting cardiac remodeling and dysfunction. The glucagon-like peptide-1 (GLP-1) has been shown exert cardioprotective effects in animals patients. This study investigates whether GLP-1 receptor agonist liraglutide inhibits abdominal aortic constriction (AAC)-induced fibrosis dysfunction through blocking Ang type 1 (AT1R) signaling.Sprague-Dawley rats were subjected sham operation banding procedure for 16 weeks. In treated rats, (0.3 mg/kg) was subcutaneously injected twice daily or telmisartan (10 mg/kg/day), AT1R blocker, administered gastric gavage.Relative with AAC, reduced protein level upregulated AT2R, as evidenced ratio AT1R/AT2R (0.59±0.04 vs. 0.91±0.06, p<0.05). Furthermore, expression angiotensin converting enzyme 2 upregulated, tissue levels malondialdehyde B-type natriuretic peptide reduced, superoxide dismutase activity increased. Along a reduction HW/BW ratio, cardiomyocyte hypertrophy inhibited. coincidence these changes, significantly decreased populations macrophages myofibroblasts myocardium, which accompanied transforming growth factor beta1, Smad2/3/4, smad7. synthesis collagen I III inhibited collagen-rich attenuated. Consistent findings, systolic function preserved, increased left ventricular pressure (110±5 99±2 mmHg, p<0.05), ejection fraction (83%±2% 69%±4%, p<0.05) shortening (49%±2% 35%±3%, Treatment provided comparable protection compared all parameters measured.Taken together, ameliorates dysfunction, potentially via suppressing AT1R-mediated events. These data indicate that might be selected an add-on drug prevent progression failure.

Language: Английский

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Sirtuin 6: A potential therapeutic target for cardiovascular diseases

Pharmacological Research, Journal Year: 2020, Volume and Issue: 163, P. 105214 - 105214

Published: Sept. 29, 2020

Language: Английский

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6-Gingerol protects against cardiac remodeling by inhibiting the p38 mitogen-activated protein kinase pathway

Acta Pharmacologica Sinica, Journal Year: 2021, Volume and Issue: 42(10), P. 1575 - 1586

Published: Jan. 18, 2021

Language: Английский

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