Engineering human ventricular heart tissue based on macroporous iron oxide scaffolds

Cmarr/miR-540-3p axis promotes cardiomyocyte maturation transition by orchestrating Dtna expression

“…Previous studies have shown that transplantation of cardiac patches with PSC-CMs promotes angiogenesis in the border zone of infarction. 27 , 28 We then investigated the effect of transplantation of cardiac patch overexpressing Cmarr on angiogenesis in mice after MI by von Willebrand Factor (vWF) and α-smooth muscle actin (α-SMA) immunostaining, and the results showed that the vascular density was increased in the Cmarr patch group ( Figure 3 J). Besides, the results of H&E staining showed that the cardiac patch was closely adhered and structurally integrated to the host myocardium and no significant insulating tissue was found in the junction 2 weeks after transplantation, indicating that the transplanted cells in the cardiac patch might be coupled to the host myocardium and achieve function recovery of the MI hearts ( Figure S4 A).…”

“…Cardiac patch acts as a promising method for the treatment of MI that could promote the maturation of PSC-CMs and improve the survival rate of transplanted cardiomyocytes in the hearts after MI. 25 , 27 , 28 , 50 , 51 Previous studies have shown that culturing in Ti 2 C-8-cryogel promotes the structural and functional maturation of PSC-CMs. Transplantation of Ti 2 C-8-cryogel cardiac patch exhibits a higher survival rate of transplanted cardiomyocytes, significantly decreases the infarct area, and improves the cardiac function of MI hearts, 25 linking the maturation of transplanted PSC-CMs to the repair efficacy of cardiac patch in the treatment of MI.…”

Inducing Endogenous Cardiac Regeneration: Can Biomaterials Connect the Dots?

“…Biomaterials, yet again, were recruited in order to overcome these hurdles. The main dogma suggests the use of porous scaffolds (Shapiro and Cohen, 1997;Dattola et al, 2019;Yang et al, 2019). Among previously mentioned advantages, such architecture also provides appropriate space and/or guiding routes for cells to penetrate the matrix.…”

Superparamagnetic iron oxide nanoparticles promote ferroptosis of ischemic cardiomyocytes

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Superparamagnetic iron oxide nanoparticles (SPION) have been widely used in the diagnosis and treatment for cardiovascular diseases. [1][2][3][4][5][6] Correspondingly, the myocardial tissue safety of SPION is becoming a bottleneck to seriously restrict its clinical translation. In recent years, in vitro and in vivo experiments have confirmed that SPION-induced oxidative stress of normal myocardium in mice, leading to myocardial cell injury, apoptosis or necrosis.

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