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Crocin, the main effective component of saffron, exerts protective effects against ischemia/reperfusion injury during strokes. However, the effects of crocin in myocardial ischemia/reperfusion injury, and the mechanisms involved, remain unknown. Pretreated with crocin for 7 days, C57BL/6N mice were subjected to 30 min of myocardial ischemia followed by 12h of reperfusion (for cardiac function and infarct size, cell apoptosis and necrosis). Neonatal mouse cardiomyocytes were subjected to 2 h of hypoxia followed by 4 h of reoxygenation. NMCM’s survival was assessed during hypoxia and reoxygenation in the presence or absence of the autophagy inhibitor 3-methyladenine or the inducer rapamycin. Western blotting was used to evaluate AMPK, Akt, and autophagy-related proteins. Autophagosome was observed using electron microscopy. In the in vivo experiment, crocin pretreatment significantly attenuated infarct size, myocardial apoptosis and necrosis, and improved left ventricular function following ischemia/reperfusion. In vitro data revealed that autophagy was induced during hypoxia, the levels of which were intensely elevated during reoxygenation. Crocin significantly promoted autophagy during ischemia, accompanied with the activation of AMPK. In contrast, crocin overtly inhibited autophagy during reperfusion, accompanied with Akt activation. Induction and inhibition of autophagy mitigated crocin induced protection against NMCMs injury during hypoxia and reoxygenation, respectively. Our data suggest that crocin demonstrated a myocardial protective effect via AMPK/mTOR and Akt/mTOR regulated autophagy against ischemia and reperfusion injury, respectively.

GE Healthcare Life Sciences and Osaka University team up to develop future leaders of Japan's life sciences sector.

Quintiles acquires Novella Clinical.

Tim Reiner joins Mundipharma's regional office.

Daiichi Sankyo to expand its collaborative drug discovery program to Germany, Switzerland, and Austria.

Eurofins Panlabs strengthens drug discovery services with GE Healthcare's Cytiva™ Cardiomyocytes.

The First Chinese Laboratory Recognized By International Olive Council (IOC).

China Kicks off Precision Medicine Research.

Chinese Researchers Find Flavonoids in Cotton Petals to Treat Alzheimer's Disease.

China Recognizes Prominent Scientists and Stresses on Innovation.

China Corporation Tencent in Kenya to Help Combat Illegal Wildlife Trade.

Catalyst Helps Convert Waste CO₂ into Fuel.

Articular Cartilage Stem Cells Participate in Cartilage Self-Repair during Early Osteoarthritis.

Chinese Scientists Develop Polygraph Based on AI Technology.

Scientists Uncover Beneficiary Effects of Dietary Iron Oxide Nanoparticles.

A New Water Robot “Born” to Detect Water Quality.

Archaeologists Discover World's Oldest Tea Buried with Ancient Chinese Emperor.

Scientists Find in situ KIT-expressing Cardiomyocytes.

Integrin CD11b Regulates Obesity-Related Insulin Resistance.

The heart is an organ with a limited capacity for regeneration and repair. In this paper, a new mathematical model is presented to study the left ventricular remodeling after myocardial infarction (MI) and followed stem cell therapeutic effort. The model represents the post-MI regeneration process of cardiomyocytes under stem cell therapy with oxygen restoration. The resulting system of nonlinear ordinary differential equations (ODE) is studied numerically in order to demonstrate the functionality and performance of the new model. The optimal time of stem cell injection for various oxygen restorations is determined. Moreover, the regeneration of cardiomyocytes is successfully correlated with improved left ventricle function observed in experiments. The proposed nonlinear ODE model is able to capture the complicated biological interactions in post-MI remodeling and can serve as a platform for in silico simulation and perturbation to optimize MI stem cell therapy.

Pluripotent stem cells offer tremendous potential for the treatment of various diseases, including cardiovascular disease. Myocardial infarction results in the almost irreversible loss of over 1 billion cardiomyocytes, with little endogenous replacement from the damaged heart. Subsequently, the quality of life of patients recovering from myocardial infarction is significantly reduced and is, to date, without an effective cure. Pluripotent stem cell-derived cardiomyocytes bring exciting potential for use in regenerative medicine therapies by replacing the damaged cells with healthy, lab-grown cardiomyocytes. However, safety concerns regarding the purity and maturity of pluripotent stem cell-derived heart muscle is currently still a significant barrier to the successful translation of lab-grown cells into patients. This chapter will review the current status of embryonic and induced pluripotent stem cell strategies to generate heart muscle, as well as discuss the currently remaining obstacles which must be overcome for the safe clinical application of stem cell therapy.

Heart disease is the primary cause of mortality and morbidity in the world. Existing therapies limit the extent of injury without structural restoration of the lost myocardial tissue. Consequently, injured myocardial tissue continues to remodel that ultimately leads to cardiac failure. Cell therapy provides a promising alternative for enhancement of cardiac structure and function, yet the mechanism explaining salutary effects remain elusive. Ability of the transplanted stem cells to adopt cardiac cell morphology dubbed as the “Transdifferentiation Hypothesis” is widely believed to be the mechanism for cell therapy. Recently, however multiple studies provide evidence that challenges the transdifferentiation hypothesis, thereby questioning the ability of transplanted stem cells to differentiate into tissue cell types. Alternatively, stem cells secrete growth factors, proteins and extracellular vesicles including exosomes that possess cardioprotective and regenerative properties, thereby forming the “Paracrine Hypothesis”. This chapter aims to summarize the cell therapy and its applications for cardiac repair and regeneration including mechanisms explaining beneficial effect of the transplanted stem cells. A particular focus will be on the emerging importance of the paracrine hypothesis and its future implication for cardiac tissue repair after injury.

Cellular reprogramming is a technique in which the identity of a mature cell is altered to generate a new cell type. This process occurs by changing the gene expression pattern of the cell, often by introducing specific transcription factors or small chemical molecules. Cellular reprogramming is a significant breakthrough in regenerative medicine and holds enormous potential in the fields of disease modeling, drug discovery, and personalized medicine. One of the most prominent examples of cellular reprogramming is the generation of induced pluripotent stem cells (iPSCs). iPSCs can differentiate into many different cell types, making them a valuable tool for regenerative medicine. Since their discovery, iPSCs have been used to generate various types of cells, such as neurons, cardiomyocytes, and hepatocytes. These cells can be used to study disease mechanisms, drug screening, and transplantation therapies. In this book chapter, we have mainly focused on methods of cellular reprogramming, various integrative and non-integrative viral and non-viral vectors, the mechanism of cellular reprogramming, its importance in disease development and regenerative medicine, and the advantages and disadvantages of cellular reprogramming.

Human pluripotent stem cells (hPSCs), including human embryonic stem cells and induced pluripotent stem cells, are a potentially inexhaustible supply of human cells because they can be propagated indefinitely while still retaining the capacity to differentiate into all somatic cell types. Hurdles facing utilization of hPSCs in regenerative medicine include lack of reliable and efficient methods to differentiate hPSCs into disease related cell lineages, including neurons, cardiac muscle cells and pancreatic beta cells. During differentiation, hPSCs make a number of developmental decisions to generate first the three germ layers (ectoderm, mesoderm and endoderm), followed by subsequent decisions to generate all of the body’s mature tissues. These differentiation processes often involve a limited set of developmental cell signaling pathways, which can be modulated by growth factors and small molecules. Therefore, common methods of differentiating hPSCs to therapeutic applicable cell lineages require application of specific combination of growth factors and/or small molecules at distinct differentiation stages. This chapter discusses recent progress in the production of therapeutically applicable cells via directed differentiation of hPSCs.