Recent evidence suggests that the heart possesses a greater regeneration capacity than previously thought. In the present study, we isolated undifferentiated precursors from the cardiac nonmyocyte cell population of neonatal hearts, expanded them in culture, and induced them to differentiate into functional cardiomyocytes. These cardiac precursors appear to express stem cell antigen-1 and demonstrate characteristics of multipotent precursors of mesodermal origin. Following infusion into normal recipients, these cells home to the heart and participate in physiological and pathophysiological cardiac remodeling. Cardiogenic differentiation in vitro and in vivo depends on FGF-2. Interestingly, this factor does not control the number of precursors but regulates the differentiation process. These findings suggest that, besides its angiogenic actions, FGF-2 could be used in vivo to facilitate the mobilization and differentiation of resident cardiac precursors in the treatment of cardiac diseases.
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http://dx.doi.org/10.1172/JCI23418 | DOI Listing |
Curr Med Chem
January 2025
Department of Cardiology, Taizhou Hospital of Zhejiang Province, affiliated to Wenzhou Medical University, Linhai, Zhejiang Province, China.
Aims: This study was to explore the relationship between plasma exosomes and Acute myocardial infarction (AMI).
Background: Acute myocardial infarction (AMI) is one of the most common cardiovascular complications. Recent studies have shown that exosomes play a crucial role in the development and progression of cardiovascular diseases.
Spinal Cord
January 2025
McKnight Brain Institute, University of Florida, Gainesville, FL, USA.
Study Design: Experimental Animal Study.
Objective: To continue validating an antibody which targets an epitope of neurofilament light chain (NF-L) only available during neurodegeneration and to utilize the antibody to describe the pattern of axonal degeneration 10 days post-unilateral C4 contusion in the rat.
Setting: University of Florida laboratory in Gainesville, USA.
Proc Natl Acad Sci U S A
January 2025
Laboratory of Obesity and Aging Research, Cardiovascular Branch, National Heart Lung and Blood Institute, NIH, Bethesda, MD 20892.
Mitochondrial endonuclease G (EndoG) contributes to chromosomal degradation when it is released from mitochondria during apoptosis. It is presumed to also have a mitochondrial function because EndoG deficiency causes mitochondrial dysfunction. However, the mechanism by which EndoG regulates mitochondrial function is not known.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio De Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) is the leading cause of dementia in elderly humans worldwide. More than 40 million people currently suffer from AD, and this prevalence tends to increase considerably in the coming decades due to increased longevity. The unfolded protein response (UPR) is an adaptive signaling mechanism that aims to maintain cell viability under misfolded protein accumulation and endoplasmic reticulum stress.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Boston University Alzheimer's Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background: Alzheimer's disease (AD) has both genetic and environmental risk factors. Gene-environment interaction may help explain some missing heritability. There is strong evidence for cigarette smoking as a risk factor for AD.
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