a-protocol-for-constructing-mouse-model-hypertensive-myocardial

A Protocol for Constructing a Mouse Model of Hypertensive Myocardial Fibrosis Using Angiotensin II

The continuous infusion of Angiotensin II (Ang II) via osmotic pumps is a widely utilized approach for establishing animal models of hypertensive ...

southwest medical university

Cardiovascular diseases (CVDs) remain the leading cause of global mortality, yet their pathogenesis has not been fully elucidated, particularly regarding the role of abnormal energy metabolism. Major outstanding questions pertain to the dynamic regulation of metabolic reprogramming and its complex interplay with mitochondrial dysfunction. Previous studies have demonstrated that the heart, as a high-energy-demand organ, relies on the dynamic equilibrium of substrates such as fatty acid (FA) and glucose to sustain adenosine triphosphate (ATP) production. Metabolic disturbances-characterized by suppressed FA oxidation and aberrant activation of glycolysis-directly contribute to the pathological progression of various CVDs, including heart failure (HF), atherosclerosis, and myocardial infarction(MI), through mechanisms involving oxidative stress, inflammatory responses, and an energy crisis. This review systematically examines the core pathways of cardiac energy metabolism (e.g., mitochondrial oxidative phosphorylation (OXPHOS), regulation of glucose and lipid metabolism) and their dysregulation in disease states, while evaluating intervention strategies targeting metabolic pathways, such as mitochondrial function enhancement and substrate utilization modulation. Future research directions emphasize the integration of metabolomics with clinical translational studies to comprehensively decipher the multidimensional regulation of metabolic networks, thereby facilitating the development of novel precision therapeutic targets.

Energy metabolism in cardiovascular diseases: unlocking the hidden powerhouse of cardiac pathophysiology.

Heart failure (HF), a serious stage of many cardiovascular illnesses associated with high morbidity and mortality, has emerged a major global public health concern worldwide. Its key pathophysiological mechanisms include cardiac remodeling, neurohormonal dysregulation and cardiac dysfunction. Despite established clinical treatments, adverse reactions and limited efficacy remain problems. In recent years, great emphasis has been paid to young blood, which is defined as blood from young people or in a youth associated physiological condition, and is abundant in various components that help maintain a youthful state of the organism. Currently, some progress has been made in the study of the anti-aging effects and mechanisms of young blood in older individuals, indicating therapeutic potential in the treatment of age-related diseases. In this paper, the major pathophysiological mechanisms of HF, the rejuvenating circulating factors in young blood and their positive effects on aging tissues are summarized. Moreover, the rejuvenating effects of young blood on the failing heart and the possible mechanisms of its action from multiple perspectives are investigated and discussed, aiming to provide theoretical foundation and potential therapeutic targets for the treatment of HF related diseases.

Article	Year
Energy metabolism in cardiovascular diseases: unlocking the hidden powerhouse of cardiac pathophysiology. Frontiers in endocrinology\| PubMed ID: 40538809	2025
Rejuvenating the failing heart: multidimensional insights into young blood-mediated anti-aging pathways. Frontiers in endocrinology\| PubMed ID: 40969375	2025

Xiaoyu Lan

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