Peyvand Parhizkar Roudsari

Cardiovascular disease is now the leading cause of adult death in the world. According to new estimates from the World Health Organization, myocardial infarction (MI) is responsible for four out of every five deaths due to cardiovascular disease. Conventional treatments of MI are taking aspirin and nitroglycerin as intermediate treatments and injecting antithrombotic agents within the first 3 h after MI. Coronary artery bypass grafting and percutaneous coronary intervention are the most common long term treatments. Since none of these interventions will fully regenerate the infarcted myocardium, there is value in pursuing more innovative therapeutic approaches. Regenerative medicine is an innovative interdisciplinary method for rebuilding, replacing, or repairing the missed part of different organs in the body, as similar as possible to the primary structure. In recent years, regenerative medicine has been widely utilized as a treatment for ischemic heart disease (one of the most fatal factors around the world) to repair the lost part of the heart by using stem cells. Here, the development of mesenchymal stem cells causes a breakthrough in the treatment of different cardiovascular diseases. They are easily obtainable from different sources, and expanded and enriched easily, with no need for immunosuppressing agents before transplantation, and fewer possibilities of genetic abnormality accompany them through multiple passages. The production of new cardiomyocytes can result from the transplantation of different types of stem cells. Accordingly, due to its remarkable benefits, stem cell therapy has received attention in recent years as it provides a drug-free and surgical treatment for patients and encourages a more safe and feasible cardiac repair. Although different clinical trials have reported on the promising benefits of stem cell therapy, there is still uncertainty about its mechanism of action. It is important to conduct different preclinical and clinical studies to explore the exact mechanism of action of the cells. After reviewing the pathophysiology of MI, this study addresses the role of tissue regeneration using various materials, including different types of stem cells. It proves some appropriate data about the importance of ethical problems, which leads to future perspectives on this scientific method.

Diabetes and heart failure, as important global issues, cause substantial expenses to countries and medical systems because of the morbidity and mortality rates. Most people with diabetes suffer from type 2 diabetes, which has an amplifying effect on the prevalence and severity of many health problems such as stroke, neuropathy, retinopathy, kidney injuries, and cardiovascular disease. Type 2 diabetes is one of the cornerstones of heart failure, another health epidemic, with 44% prevalence. Therefore, finding and targeting specific molecular and cellular pathways involved in the pathophysiology of each disease, either in diagnosis or treatment, will be beneficial. For diabetic cardiomyopathy, there are several mechanisms through which clinical heart failure is developed; oxidative stress with mediation of reactive oxygen species (ROS), reduced myocardial perfusion due to endothelial dysfunction, autonomic dysfunction, and metabolic changes, such as impaired glucose levels caused by insulin resistance, are the four main mechanisms. In the field of oxidative stress, advanced glycation end products (AGEs), protein kinase C (PKC), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) are the key mediators that new omics-driven methods can target. Besides, diabetes can affect myocardial function by impairing calcium (Ca) homeostasis, the mechanism in which reduced protein phosphatase 1 (PP1), sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a), and phosphorylated SERCA2a expressions are the main effectors. This article reviewed the recent omics-driven discoveries in the diagnosis and treatment of type 2 diabetes and heart failure with focus on the common molecular mechanisms.

Abstract Purpose Glucagon-like peptide-1 (GLP-1) receptor agonists have shown potential in managing eating disorders (EDs). Recent studies highlight their effects on pathophysiological pathways, indicating their therapeutic promise, particularly for binge eating disorder (BED). This systematic review evaluates the therapeutic effects of GLP-1 agonists on BED, focusing on weight management and eating behaviors. Methods A systematic search of PubMed, Scopus, Web of Science, and the Cochrane Library, along with manual searches, identified studies assessing GLP-1 agonists in BED patients up to November 8, 2024. Observational studies and clinical trials meeting inclusion criteria were analyzed. Results Five studies (182 participants) were included. Patients receiving GLP-1 agonists experienced greater weight loss (− 3.81 kg; 95% CI − 5.14 to − 2.49; p < 0.01, I 2 : 59.88%) compared to controls. GLP-1 agonists significantly reduced BMI (− 1.48 kg/m 2 ) and waist circumference (− 3.14 cm). Binge Eating Scale (BES) scores improved significantly (− 8.14 points; 95% CI − 13.13 to − 3.15; p < 0.01), though heterogeneity was noted. Conclusions This review underscores the potential role of GLP-1 agonists in BED management. However, given the limited data, especially concerning EDs other than BED and the long-term effects of these medications, further comprehensive clinical trials are recommended to evaluate the impact of various GLP-1 agonists on different EDs across diverse demographic groups. Level of evidence Level I, randomized controlled trials.