Myocardial infarction (MI) is one of the leading causes of death worldwide, with its high incidence and mortality posing a significant threat to human health. Despite some progress in the treatment of myocardial infarction, mortality rates remain alarmingly high. Adult mammals have limited myocardial regenerative capacity, and extensive cell death caused by myocardial ischemia severely impairs cardiac function, leading to heart failure or death. In contrast, neonatal myocardium possesses a robust regenerative ability, which gradually diminishes after birth. The loss of cardiomyocyte regenerative capacity is often accompanied by a shift in energy metabolism-from reliance on glucose (glycolysis) to fatty acid oxidation. This metabolic reprogramming significantly impacts CM proliferation. Long non-coding RNAs (lncRNAs) orchestrate cardiac regeneration through epigenetic control (e.g., Bvht/PRC2-mediated silencing), metabolic reprogramming (e.g., GATA6-AS1 suppression of FAO), and miRNA sponging (e.g., CAREL sequestration of miR-296). However, our understanding of the metabolic determinants and pathways that promote myocardial regeneration after myocardial infarction is still insufficient. This review investigates the interplay between lncRNAs and metabolic reprogramming in cardiovascular function, aiming to identify novel therapeutic targets and strategies to enhance myocardial regeneration post-MI.
Background: Obesity is a major contributor to metabolic dysfunction and is driven by complex genetic, behavioral, and physiological factors. Neuropeptide FF receptor 2 (NPFFR2) has been implicated in regulating feeding behavior, as well as energy and glucose homeostasis. However, its precise role in obesity and metabolic disorders remains unclear. This study aimed to investigate the systemic role of NPFFR2 in obesity-induced metabolic dysfunction.
Material and methods: The role of NPFFR2 was examined using wild-type and Npffr2-overexpressing transgenic mice subjected to 15 weeks of high-fat high-sucrose diet to induce obesity. Systemic, tissue-specific, and serum metabolic profiles were analyzed, with a particular focus on lipid abnormalities in the liver and adipose tissues.
Results: Npffr2 overexpression exacerbated obesity-induced metabolic dysfunction, including accelerated body weight gain, impaired glucose homeostasis, altered fat composition, adipose tissue inflammation, and dysregulated lipid metabolism. In addition, hypertrophy of both hepatocytes and adipocytes was aggravated in Npffr2-overexpressing mice, collectively contributing to excessive energy storage and reduced metabolic efficiency.
Conclusions: These findings suggest that NPFFR2 may contribute to the regulation of energy balance and lipid metabolism, potentially via central regulatory pathways. These findings highlight the need for mechanistic studies to clarify its region-specific roles and therapeutic potential in metabolic disorders.

