The pluripotent role of exosomes in mediating non-coding RNA in ventricular remodeling after myocardial infarction

Qi, Zhongwen; Wu, Dan; Li, Meng; Yan, Zhipeng; Yang, Xinggang; Ji, Nan; Wang, Yueyao; Zhang, Junping

doi:10.1016/j.lfs.2020.117761

Cited by 13 publications

(7 citation statements)

References 114 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Exosomes have emerged as a promising therapy for promoting cardiac repair ( 30 ), with anti-apoptotic ( 31 ), anti-inflammatory ( 32 ), and pro-angiogenic activities ( 33 ). These effects have important clinical significance for improving cardiac function.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rh2 Inhibits NLRP3 Inflammasome Activation and Improves Exosomes to Alleviate Hypoxia-Induced Myocardial Injury

Yan

Wang

et al. 2022

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

The inflammatory microenvironment after acute myocardial infarction (MI) is a key limiting factor in the clinical application of stem cell transplantation and paracrine exosome therapy. Qishen Yiqi Pills contain a saponin ingredient called Ginsenoside Rh2 (Rh2) which exhibits a certain therapeutic effect on MI. However, the mechanism by which Rh2 alleviates the inflammatory microenvironment and improves the therapeutic efficiency of exosomes remains enigmatic. Here, we found that Rh2 attenuated the adverse effect of oxygen-glucose deprivation (OGD)-induced cellular injury, an in vitro pathological model of MI. Confocal microscopy revealed that DiI-labeled BMSCs-derived exosomes exhibited an increased homing ability of cardiomyocytes, which, in turn, inhibited the nuclear translocation of NF-κB p65 and NLRP3 inflammasome activation, thereby alleviating the inflammatory microenvironment and further facilitating the homing of exosomes to cardiomyocytes by forming a feed-forward enhancement loop. Additionally, we found that Rh2 could regulate the HMGB1/NF-κB signaling pathway to improve the OGD environment of cardiomyocytes, increasing the efficiency of the feed-forward loop. In conclusion, we found that Rh2 can improve the inflammatory microenvironment by enhancing the protection of exosomes against myocardial injury, providing new insights into the indirect modification of exosomes by Rh2 in MI treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rh2 Inhibits NLRP3 Inflammasome Activation and Improves Exosomes to Alleviate Hypoxia-Induced Myocardial Injury

Yan

Wang

et al. 2022

Front. Immunol.

Self Cite

View full text Add to dashboard Cite

show abstract

“…Therefore, the BMSC-derived exosomes could constitute a viable treatment approach for AF. The protective effect of exosomes from different cells may be related to cytoprotective factors [ 30 , 31 ]. For instance, Wang et al [ 32 ] showed that MSC exosomes carrying microRNA-671 inhibit cardiomyocyte apoptosis, myocardial fibrosis, and inflammation by inactivating the TGFBR2/Smad2 axis.…”

Section: Discussionmentioning

confidence: 99%

Exosomes from Bone Marrow Mesenchymal Stem Cells with Overexpressed Nrf2 Inhibit Cardiac Fibrosis in Rats with Atrial Fibrillation

Fan

et al. 2022

Cardiovascular Therapeutics

View full text Add to dashboard Cite

Background. Even though nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling has been associated with the pathogenesis of multiple heart conditions, data on roles of Nrf2 within atrial fibrillation (AF) still remain scant. The present investigation had the aim of analyzing Nrf2-overexpressing role/s upon bone mesenchymal stem cell- (BMSC-) derived exosomes in rats with AF. Methods. Exosomes were collected from control or Nrf2 lentivirus-transduced BMSCs and then injected into rats with AF through the tail vein. AF duration was observed using electrocardiography. Immunohistochemical staining was then employed for assessing Nrf2, HO-1, α-SMA, collagen I, or TGF-β1 expression profiles within atrial myocardium tissues. Conversely, Masson staining was utilized to evaluate atrial fibrosis whereas apoptosis within myocardia was evaluated through TUNEL assays. In addition, TNF-α, IL-1β, IL-4, or IL-10 serum expression was assessed through ELISA. Results. Results of the current study showed significant downregulation of Nrf2/HO-1 within AF rat myocardia. It was found that injection of the control or Lv-Nrf2 exosomes significantly alleviated and lowered AF timespans together with reducing cardiomyocyte apoptosis. Moreover, injection of Lv-Nrf2 exosomes essentially lowered AF-driven atrial fibrosis and also inhibited inflammatory responses in the rats with AF. Conclusion. Delivery of BMSC-derived exosomes using overexpressed Nrf2 inhibited AF-induced arrhythmias, myocardial fibrosis, apoptosis, and inflammation via Nrf2/HO-1 pathway triggering.

show abstract

“…An extremely complex pathogenesis of this process includes myocardial hypertrophy, brosis, in ammation, autophagy and metabolic malfunction 19 . It has been recently demonstrated that exosomes are considered as the main mediators of intercellular communication in the myocardium, which may attenuate the development of detrimental structural changes and the consequent heart failure after MI 20 . Thus, the presence of exosomes likely contributes to inhibition of brosis, promotion of angiogenesis and alleviation of in ammation and pyroptosis, by translocation of intercellular molecules, proteins, and organelles.…”

Section: Discussionmentioning

confidence: 99%

Exosomal hsa_circ_0007047 Attenuates Pos-myocardial Infarction Remodeling by Promoting Angiogenesis via miR-1178-3p/PDPK1 Axis

Mao¹,

Liang²,

Yu³

et al. 2021

Preprint

View full text Add to dashboard Cite

Emerging studies indicate that exosomes and their inner noncoding RNAs, especially circular RNAs (circRNAs), play key roles in gene regulatory network and cardiovascular repair. However, our understanding of exosomal circRNAs on cardiac remodeling after myocardial infarction (MI) remains limited. In the present study, exosomes were harvested from the serum of patients with and without postinfarction cardiac remodeling. The results showed that the level of hsa_circ_0007047 was significantly downregulated in serum exosome of patients with the adverse cardiac remodeling when compared with those without post-MI remodeling or normal subjects. Loss-of-function approaches in vitro established that exosomal hsa_circ_0007047 robustly promoted angiogenesis and stimulated of cultured human vascular smooth muscle cells proliferation and migration. Accordingly, overexpression of exosomal hsa_circ_0007047 in mice significantly attenuated MI-induced myocardial fibrosis and left ventricular dysfunction, accompanied by a larger functional capillary network at the border zone. Further exploration of the downstream target gene indicated that hsa_circ_0007047 acts as a competing endogenous RNA by directly binding to miR-1178-3p and thereby inducing transcription of its target gene phosphoinositide-dependent kinase-1 (PDPK1), a critical positive regulatory factor of angiogenesis. Together, our results revealed that exosomal hsa_circ_0007047 attenuated detrimental post-MI remodeling via miR-1178-3p/PDPK1 axis, which facilitated revascularization, ultimately improved the cardiac function.

show abstract

The pluripotent role of exosomes in mediating non-coding RNA in ventricular remodeling after myocardial infarction

Cited by 13 publications

References 114 publications

Ginsenoside Rh2 Inhibits NLRP3 Inflammasome Activation and Improves Exosomes to Alleviate Hypoxia-Induced Myocardial Injury

Ginsenoside Rh2 Inhibits NLRP3 Inflammasome Activation and Improves Exosomes to Alleviate Hypoxia-Induced Myocardial Injury

Exosomes from Bone Marrow Mesenchymal Stem Cells with Overexpressed Nrf2 Inhibit Cardiac Fibrosis in Rats with Atrial Fibrillation

Exosomal hsa_circ_0007047 Attenuates Pos-myocardial Infarction Remodeling by Promoting Angiogenesis via miR-1178-3p/PDPK1 Axis

Contact Info

Product

Resources

About