MSCs-Derived Extracellular Vesicles Carrying miR-212-5p Alleviate Myocardial Infarction-Induced Cardiac Fibrosis via NLRC5/VEGF/TGF-β1/SMAD Axis

Qige Huxin Formula Attenuates Isoprenaline-Induced Cardiac Fibrosis in Mice via Modulating Gut Microbiota and Protecting Intestinal Integrity

“…ese substances, as proinflammatory mediators, stimulate the proliferation and activation of the resident fibroblasts and their transformation into myofibroblasts [36], thus promoting the deposition of matrix proteins in the ECM. Previous studies have exhibited that decreasing proinflammatory factors can ameliorate myocardial fibrosis [37][38][39]. In our present study, the serum levels of proinflammatory cytokines, including TNF-α, IL-1β, and IL-6, were increased significantly in the model group.…”

Exosomes and Exosomal Cargos: A Promising World for Ventricular Remodeling Following Myocardial Infarction

“… 138 , 139 A cardiac fibrosis model was established in C57BL/6 male mice using the left anterior descending (LAD) coronary artery ligation method and the study discovered miR-212-5p, enriched in MSC-EVs, exerts an anti-fibrotic effect by inhibiting hypoxia-mediated activation of CFs via targeting the TGF-β1/Smad pathway. 140 Similarly, exosomal miR-30d promotes the proliferation of CFs by targeting integrin α-5 (itga5) directly and inhibiting the TGF-β1/Smad pathway, the key profibrotic pathway. 141 Moreover, Ramanujam et al indicated that macrophage miR-21 is necessary to maintain the proinflammatory phenotype of M1 macrophages and activate fibroblasts into myofibroblasts, while further study demonstrated miR-21-5p derived from M1 exosomes induces cardiac fibrosis via targeting tissue inhibitor of metalloproteinase 3 (TIMP3).…”

From cerebral ischemia towards myocardial, renal, and hepatic ischemia: Exosomal miRNAs as a general concept of intercellular communication in ischemia-reperfusion injury

“… 106 , 107 Exosomes, in the meantime, could be taken up by neighboring or distant myocardial cells, given their various targets, which they modulate by posttranscriptional regulation of gene expression; miRNAs loaded into exosomes are potent repair factors. 108 There is increasing evidence that miRNAs are selectively enriched in exosomes, exerting biological functions via modulating specific aspects of myocardial ischemia and, as such, participating in cardiomyocyte survival, cardiac functional recovery, inflammatory responses, and angiogenesis, 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 as indicated in Table 2 and Figure 4 and further discussed in the following sections.…”

“…As such, a series of miRNAs were shuttled via exosomes, including miR-21, miR-98-5p, miR-25, miR-30e, miR-125b, miR-126, miR-4732-3p, miR-146a, miR-185, miR-150-5p, miR-210, miR-212-5p, miR-31, miR-486-5p, miR-338, and miR-671, which, collected from MSCs, cardiac progenitor cells, endothelial cells, endothelial progenitor cells, or patient serum, promoted cardiomyocyte survival by downregulating miRNA targets including PDCD4, FASL, TLR4, PTEN, LOX1, p53, BAK, or SOCS2. 112 , 114 , 117 , 118 , 120 , 123 , 124 , 127 , 129 , 130 , 131 , 132 , 133 , 137 , 138 , 140 , 141 , 142 In addition to the effect on cardiomyocyte survival, several miRNAs, namely miR-24, miR-98-5p, miR-125b, miR-126, miR-133a-3p, miR-150-5p, miR-338, miR-4732-3p, miR-31, miR-210, and miR-486-5p, loading into exosomes from cardiomyocytes, MSCs, or endothelial cells were identified to promote cardiac function recovery by promoting cardiomyocyte survival, anti-inflammation, angiogenesis, or anti-fibrosis. 114 , 117 , 118 , 120 , 124 , 127 , 131 , 138 , 141 , 142 Suggestively, exosomal miRNAs play momentous roles in coordinating responses to cardioprotective effects, i.e., by promoting cardiomyocyte survival and cardiac functional recovery.…”

“…As such, a series of miRNAs were shuttled via exosomes, including miR-21, miR-98-5p, miR-25, miR-30e, miR-125b, miR-126, miR-4732-3p, miR-146a, miR-185, miR-150-5p, miR-210, miR-212-5p, miR-31, miR-486-5p, miR-338, and miR-671, which, collected from MSCs, cardiac progenitor cells, endothelial cells, endothelial progenitor cells, or patient serum, promoted cardiomyocyte survival by downregulating miRNA targets including PDCD4, FASL, TLR4, PTEN, LOX1, p53, BAK, or SOCS2. 112,114,117,118,120,123,124,127,[129][130][131][132][133]137,138,[140][141][142] In addition to Molecular Therapy: Nucleic Acids Vol. 29 September 2022…”