Despite an improvement in the therapeutic strategies available for an acute ischemic event, cardiac disease is still the principal cause of morbidity and mortality in Western societies. A shift from acute towards more chronic heart disease due to atherosclerotic disease has been recognized. Modification of adaptive capacities of the cardiac muscle after damage remains a key component in the prevention of chronic cardiac disease, such as overt heart failure. It has recently been demonstrated that local insulin-like growth factor (IGF)-1 homeostasis in the cardiac tissue is closely involved in postischemic adaptation, such as the process of remodeling. Both experimental and clinical data support the theory that IGF-1 plays a key role in the adaptive response of the myocardium during both acute myocardial ischemia and chronic myocardial failure, regulating left ventricular remodeling and thereby restoring left ventricular architecture. This eventually leads to improvement in the function of the failing heart. While most experimental data support the beneficial role of IGF-1 in restoring architecture and function of the failing heart, clinical trials investigating the role of IGF-1 treatment of patients in cardiac failure show conflicting results. In this bench-to-bedside review, the authors aim to highlight recent advances in knowledge of the role of paracrine and autocrine IGF balances during postischemic cardiac adaptation, in order to present possible new initiatives concerning therapeutic strategies in maladaptive cardiac performance, such as the syndrome of heart failure.
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http://dx.doi.org/10.2217/14796678.1.4.479 | DOI Listing |
Front Microbiol
January 2025
Department of Medicine, Qinghai University, Xining, Qinghai, China.
Objective: This study aimed to investigate the potential relation between the retarded growth of skeletal muscle (SM) and dysbiosis of gut microbiota (GM) in children with asthma, and to explore the potential action mechanisms of traditional pediatric massage (TPM) from the perspective of regulating GM and short-chain fatty acids (SCFAs) production by using an adolescent rat model of asthma.
Methods: Male Sprague-Dawley rats aged 3weeks were divided randomly into the 5 groups (n=6~7) of control, ovalbumin (OVA), OVA + TPM, OVA + methylprednisolone sodium succinate (MP) and OVA + SCFAs. Pulmonary function (PF) was detected by whole body plethysmograph, including enhanced pause and minute ventilation.
Front Cell Neurosci
January 2025
Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, China.
Alzheimer's disease (AD) is the most prevalent type of dementia. Treatments for AD do not reverse the loss of brain function; rather, they decrease the rate of cognitive deterioration. Current treatments are ineffective in part because they do not address neurotrophic mechanisms, which are believed to be critical for functional recovery.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
Department of Pediatric Endocrinology and Rheumatology, Institute of Pediatrics, Poznan University of Medical Sciences, Poznan, Poland.
Background: Loeys-Dietz syndrome (LDS) is a clinically and genetically heterogeneous, autosomal dominant aortic aneurysm syndrome with widespread systemic involvement. We present the case of a 16.5-year-old girl with LDS type 2 (LDS2) caused by a heterozygous pathogenic variant, c.
View Article and Find Full Text PDFEur J Med Res
January 2025
School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
MicroRNAs (miRNAs), also known as microribonucleic acids, are small molecules found in specific tissues that are essential for maintaining proper control of genes and cellular processes. Environmental factors, such as physical exercise, can modulate miRNA expression and induce targeted changes in gene transcription. This article presents an overview of the present knowledge on the principal miRNAs influenced by physical activity in different tissues and bodily fluids.
View Article and Find Full Text PDFJ Sport Health Sci
January 2025
Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia; Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC 3086, Australia; Department of Diabetes, Central Clinical School, Monash University, Clayton, VIC 3800, Australia; Department of Cardiometabolic Health, University of Melbourne, Melbourne, VIC 3010, Australia; Department of Cardiovascular Research, Translation and Implementation, La Trobe University, Bundoora, VIC 3086, Australia; Department of Physiology and Department of Medicine Alfred Hospital, Monash University, Clayton, VIC 3800, Australia; Heart Research Institute, Newtown, NSW 2042, Australia. Electronic address:
Background: Elucidating mechanisms underlying atrial myopathy, which predisposes individuals to atrial fibrillation (AF), will be critical for preventing/treating AF. In a serendipitous discovery, we identified atrial enlargement, fibrosis, and thrombi in mice with reduced phosphoinositide 3-kinase (PI3K) in cardiomyocytes. PI3K(p110α) is elevated in the heart with exercise and is critical for exercise-induced ventricular enlargement and protection, but the role in the atria was unknown.
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