Acquired cardiovascular diseases such as coronary heart disease, peripheral artery disease and related vascular problems contribute to more than one-third of worldwide morbidity and mortality. In many instances, particularly in the under developed world, cardiovascular diseases are diagnosed at a late stage limiting the scope for improving outcomes. A range of therapies already exist for established cardiovascular disease, although there is significant interest in further understanding disease pathogenesis in order to improve diagnosis and achieve primary and secondary therapeutic goals. The urocortins are a group of recently defined peptide members of the corticotrophin-releasing factor family. Previous pre-clinical work and human association studies suggest that urocortins have potential to exert some beneficial and other detrimental effects on the heart and major blood vessels. More current evidence however favours beneficial effects of urocortins, for example these peptides have been shown to inhibit production of reactive oxygen species and vascular cell apoptosis, and thus may have potential to antagonise the progression of cardiovascular disease. This review summarises published data on the potential role of urocortins in cardiovascular disease.
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http://dx.doi.org/10.1016/j.yjmcc.2011.06.002 | DOI Listing |
PLoS One
January 2025
Graduate Institute of Injury Prevention and Control, College of Public Health, Taipei Medical University, Taipei, Taiwan.
Background: Global populations are aging, and the numbers of stroke survivors is increasing. Consequently, the need for caregiver support has increased. Because of this and demographic and socioeconomic changes, foreign caregivers are increasingly in demand in many developed countries.
View Article and Find Full Text PDFBackground: Poststroke depression (PSD) is a highly prevalent and serious mental health condition affecting a significant proportion of stroke survivors worldwide. While its exact causes remain under investigation, managing PSD presents a significant challenge.
Aim: This study aimed to evaluate the prevalence and predictors of depression among Bangladeshi stroke victims.
Proc Natl Acad Sci U S A
January 2025
Department of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037.
is one of the three most frequently mutated genes in age-related clonal hematopoiesis (CH), alongside and (. CH can progress to myeloid malignancies including chronic monomyelocytic leukemia (CMML) and is also strongly associated with inflammatory cardiovascular disease and all-cause mortality in humans. DNMT3A and TET2 regulate DNA methylation and demethylation pathways, respectively, and loss-of-function mutations in these genes reduce DNA methylation in heterochromatin, allowing derepression of silenced elements in heterochromatin.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Institute of Optical Materials and Chemical Biology, Guangxi Key Laboratory of Electrochemical Energy Materials, School of Chemistry and Chemical Engineering, Guangxi University, Nanning 530004, Guangxi, People's Republic of China.
Monitoring subcellular organelle dynamics in real time and precisely assessing membrane heterogeneity in living cells are very important for studying fundamental biological mechanisms and gaining a comprehensive understanding of cellular processes. However, there remains a shortage of effective tools for these purposes. Herein, we propose a strategy to develop the exchangeable water-sensing probeAPBD for time-lapse imaging of dynamics in cellular membrane-bound organelle morphology with structured illumination microscopy at the nanoscale.
View Article and Find Full Text PDFProc 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.
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