Cardiosome-mediated protection in myocardial ischemia

Arroyo-Campuzano, Miguel; Aurora, Gil-Hernández; Alejandro, Silva-Palacios

doi:10.1016/j.cca.2023.117374

Cited by 2 publications

(3 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Besides hypoxemia, these cells increase EV secretion under several other stress signals. In addition to protection against apoptosis, cardiosomes promote cell proliferation and angiogenesis when incubated with endothelial cells and improve dysfunctional mitochondria after periods of hypoxia [64]. Cardiosomes extracted from post-ischemic conditioned cells appear to play a role in remodeling repair and protection against reperfusion injury.…”

Section: Vesicle-derived Signaling For Cardiac Regenerationmentioning

confidence: 99%

“…Cardiosomes containing miR-424-3p, which regulates Ras-related protein signaling, elicit regenerative responses against hypoxia/reoxygenation [67]. In addition, cardiosomes facilitate macrophage polarization, favoring the reparative phenotype and protecting against reperfusion injury [64].…”

Section: Vesicle-derived Signaling For Cardiac Regenerationmentioning

confidence: 99%

“…However, the isolation and manipulation of these EVs have proven difficult, highlighting a need for further investigations [63]. Importantly, cardiosomes serve as valuable biomarkers, aiding in early detection and intervention of MI [64]. In patients with acute MI or other acute coronary syndromes, miR-1 and miR-133a (cardiosome-derived) were significantly elevated [68].…”

Section: Vesicle-derived Signaling For Cardiac Regenerationmentioning

confidence: 99%

See 2 more Smart Citations

Engineered Vesicles and Hydrogel Technologies for Myocardial Regeneration

Ghassemi,

Inouye,

Takhmazyan

et al. 2023

Gels

View full text Add to dashboard Cite

Increased prevalence of cardiovascular disease and potentially life-threatening complications of myocardial infarction (MI) has led to emerging therapeutic approaches focusing on myocardial regeneration and restoration of physiologic function following infarction. Extracellular vesicle (EV) technology has gained attention owing to the biological potential to modulate cellular immune responses and promote the repair of damaged tissue. Also, EVs are involved in local and distant cellular communication following damage and play an important role in initiating the repair process. Vesicles derived from stem cells and cardiomyocytes (CM) are of particular interest due to their ability to promote cell growth, proliferation, and angiogenesis following MI. Although a promising candidate for myocardial repair, EV technology is limited by the short retention time of vesicles and rapid elimination by the body. There have been several successful attempts to address this shortcoming, which includes hydrogel technology for the sustained bioavailability of EVs. This review discusses and summarizes current understanding regarding EV technology in the context of myocardial repair.

show abstract

Section: Vesicle-derived Signaling For Cardiac Regenerationmentioning

confidence: 99%

Section: Vesicle-derived Signaling For Cardiac Regenerationmentioning

confidence: 99%

Section: Vesicle-derived Signaling For Cardiac Regenerationmentioning

confidence: 99%

See 1 more Smart Citation

Engineered Vesicles and Hydrogel Technologies for Myocardial Regeneration

Ghassemi,

Inouye,

Takhmazyan

et al. 2023

Gels

View full text Add to dashboard Cite

show abstract

Cardiomyocyte‐derived small extracellular vesicle‐transported let‐7b‐5p modulates cardiac remodeling via TLR7 signaling pathway

Zhang,

Cui,

Zhao

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

Cardiac remodeling is the major pathological change of heart failure. And let‐7 family has been implicated in the development and pathogenesis of cardiovascular diseases. However, the mechanisms underlying let‐7b‐5p‐mediated cellular pathogenesis of cardiac remodeling are not well understood. The present study aimed to explore the effects of let‐7b‐5p on cardiac remodeling and the corresponding regulatory mechanism. In vivo results indicated that cardiac let‐7b‐5p was upregulated in the mouse model of Angiotensin II (Ang II)‐induced cardiac remodeling. Additionally, let‐7b‐5p knockdown ameliorated the effects of Ang II‐induced cardiac remodeling, whereas let‐7b‐5p overexpression facilitated cardiac remodeling. In vitro, let‐7b‐5p mimics induced cardiomyocyte hypertrophy, fibroblast transdifferentiation, and the expression of inflammatory factors in neonatal mouse cardiomyocytes (NMCMs), neonatal mouse cardiac fibroblasts (NMCFs), and bone marrow‐derived macrophages (BMDMs), respectively. Furthermore, let‐7b‐5p exerted its cardiac pro‐remodeling effects at least partially through a small extracellular vesicle (SEV)‐based delivery strategy. We found that let‐7b‐5p was enriched in SEVs derived from Ang II‐treated NMCMs (NMCM‐SEV) but not from Ang II‐treated NMCFs (NMCF‐SEV). Mechanistic analyses revealed that NMCM‐SEV promoted TLR7 and MyD88 expression, which increased NF‐κB phosphorylation levels. Knockdown of let‐7b‐5p, TLR7 or MyD88 in NMCMs, NMCFs, and BMDMs abolished the cardiac pro‐remodeling effects of NMCM‐SEV. These results uncover that let‐7b‐5p‐containing NMCM‐SEVs promote cardiac remodeling via the TLR7/MyD88/NF‐κB pathway, implicating let‐7b‐5p as a potential therapeutic target for heart failure.

show abstract

Cardiosome-mediated protection in myocardial ischemia

Cited by 2 publications

References 75 publications

Engineered Vesicles and Hydrogel Technologies for Myocardial Regeneration

Engineered Vesicles and Hydrogel Technologies for Myocardial Regeneration

Cardiomyocyte‐derived small extracellular vesicle‐transported let‐7b‐5p modulates cardiac remodeling via TLR7 signaling pathway

Contact Info

Product

Resources

About