Human heart assembloids with autologous tissue-resident macrophages recreate physiological immuno-cardiac interactions.

Interactions between the developing heart and the embryonic immune system are essential for proper cardiac development and maintaining homeostasis, with disruptions linked to various diseases. While human pluripotent stem cell (hPSC)-derived organoids are valuable models for studying human organ function, they often lack critical tissue-resident immune cells. Here, we introduce an advanced human heart assembloid model, termed hHMA (human heart-macrophage assembloid), which fully integrates autologous cardiac tissue- resident macrophages (MPs) with pre-existing human heart organoids (hHOs).

A patterned human primitive heart organoid model generated by pluripotent stem cell self-organization.

Pluripotent stem cell-derived organoids can recapitulate significant features of organ development in vitro. We hypothesized that creating human heart organoids by mimicking aspects of in utero gestation (e.g.

Biotechnological advances and applications of human pluripotent stem cell-derived heart models.

In recent years, significant biotechnological advancements have been made in engineering human cardiac tissues and organ-like models. This field of research is crucial for both basic and translational research due to cardiovascular disease being the leading cause of death in the developed world. Additionally, drug-associated cardiotoxicity poses a major challenge for drug development in the pharmaceutical and biotechnological industries.

Direct Cardiac Epigenetic Reprogramming through Codelivery of 5'Azacytidine and miR-133a Nanoformulation.

Direct reprogramming of cardiac fibroblasts to induced cardiomyocytes (iCMs) is a promising approach to cardiac regeneration. However, the low yield of reprogrammed cells and the underlying epigenetic barriers limit its potential. Epigenetic control of gene regulation is a primary factor in maintaining cellular identities.

Scaffold mediated delivery of dual miRNAs to transdifferentiate cardiac fibroblasts.

The standard scaffold-mediated delivery of drugs/biomolecules has been successful due to the unique attributes of scaffolds, specifically the electrospun polymeric scaffolds that mimic ECM are well suited for advanced regenerative applications. Cardiac tissue engineering includes the interpretation of cellular and molecular mechanisms concerning heart regeneration and identifying an efficient reprogramming strategy to overcome the limitation of delivery systems and enhance the reprogramming efficiency. This study is a step towards developing a functional scaffold through a parallel interpretation of electrospun PLLA scaffolds with two distinct topologies to achieve sustained delivery of two muscle-specific microRNAs (miR-1 and miR-133a) to directly reprogram the adult human cardiac fibroblasts into cardiomyocyte-like cells.

Direct Cardiac Reprogramming with Engineered miRNA Scaffolds.

Ischemic heart disease is a predominant cause of death worldwide. The loss or death of cardiomyocytes due to restricted blood flow often results in a cardiac injury. Myofibroblasts replace these injured cardiomyocytes to preserve structural integrity.

ECM Mimetic Electrospun Porous Poly (L-lactic acid) (PLLA) Scaffolds as Potential Substrates for Cardiac Tissue Engineering.

Cardiac tissue engineering (CTE) aims to generate potential scaffolds to mimic extracellular matrix (ECM) for recreating the injured myocardium. Highly porous scaffolds with properties that aid cell adhesion, migration and proliferation are critical in CTE. In this study, electrospun porous poly (l-lactic acid) (PLLA) porous scaffolds were fabricated and modified with different ECM derived proteins such as collagen, gelatin, fibronectin and poly-L-lysine.

Vesicular systems employing natural substances as promising drug candidates for MMP inhibition in glioblastoma: A nanotechnological approach.

Glioblastoma multiforme (GBM), one of the most lethal Brain tumors, characterized by its high invasive nature and increased mortality rates forms a major bottleneck in transport of therapeutics across the Blood Brain Barrier (BBB). Matrix metalloproteinases (MMPs) are classified as enzymes, which are found to be up regulated in the Glioma tumor microenvironment and thus can be considered as a target for inhibition for curbing GBM. Many chemotherapeutics and techniques have been employed for inhibiting MMPs till now but all of them failed miserably and were withdrawn in clinical trials due to their inability in restricting the tumor growth or increasing the overall survival rates.