Diabetic foot ulcer's impaired wound healing, which leads to the development of chronic non-healing wounds and ultimately amputation, is a major problem worldwide. Although recently endothelial progenitor cell-derived cell therapy has been used as a therapeutic intervention to treat diabetic wounds, thereby promoting neovascularization, the results, however, are not satisfactory. In this article, we have discussed the several steps that are involved in the neovascularization process, which might be impaired during diabetes. In addition, we have also discussed the reported possible interventions to correct these impairments. Thus, we have summarized neovascularization as a process with a coordinated sequence of multiple steps and thus, there is the need of a combined therapeutic approach to achieve better treatment outcomes.
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http://dx.doi.org/10.1089/cell.2016.0050 | DOI Listing |
Alzheimers Dement
December 2024
The Jackson Laboratory, Bar Harbor, ME, USA.
Background: Data from human and model organism studies suggest that genetic background influences susceptibility and resilience to Alzheimer's Disease (AD) neuropathology. We previously showed that, wild-derived PWK/PhJ (PWK) mice carrying the APP/PS1 transgene (PWK.APP/PS1) exhibit cognitive and synaptic resilience compared to traditionally-studied B6.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Department of Physiology, Anatomy & Genetics, University of Oxford, Oxford, UK.
During embryogenesis, endothelial cells (ECs) are generally described to arise from a common pool of progenitors termed angioblasts, which diversify through iterative steps of differentiation to form functionally distinct subtypes of ECs. A key example is the formation of lymphatic ECs (LECs), which are thought to arise largely through transdifferentiation from venous endothelium. Opposing this model, here we show that the initial expansion of mammalian LECs is primarily driven by the in situ differentiation of mesenchymal progenitors and does not require transition through an intermediate venous state.
View Article and Find Full Text PDFAm J Physiol Gastrointest Liver Physiol
January 2025
Wake Forest Institute for Regenerative Medicine, Wake Forest Baptist Medical Center, Winston-Salem, North Carolina, USA.
This study aimed to determine if local injection of CXCL12 reduces sphincter fibrosis, restores sphincter muscle content, vascularization, and innervation, and recruits progenitor cells in a rabbit model of anal sphincter injury and incontinence. Adult female rabbits were assigned to 3 groups: uninjured/no treatment (control), injured/treated (treated), and injured/no treatment (untreated) (n=4 each). Injured groups were anesthetized and a section of external anal sphincter was removed at the 9:00 o'clock position.
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
Department of Cardiology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Despite improvements in clinical outcomes of acute myocardial infarction (AMI), mortality rates remain high, indicating the need for further understanding of the pathogenesis and developing more effective cardiac protection strategies. Extracellular vesicles (EVs) carry proteins and noncoding RNAs (ncRNAs) derived from different cardiac cell populations, mainly including cardiomyocytes, endothelial cells, endothelial progenitor cells, cardiac progenitor cells, cardiosphere-derived cells, immune cells, fibroblasts and cardiac telocytes have vital roles under both physiological and pathological process such as myocardial infarction (MI). The content of EVs can also indicate the status of their parental cells and serve as a biomarker for monitoring the risk of cardiac injury.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Escuela de Tecnología Médica, Facultad de Medicina y Ciencia, Universidad San Sebastián, Santiago, Chile.
Preeclampsia (PE) is a complex pregnancy syndrome characterized by hypertension with or without proteinuria, affecting 2-6% of pregnancies globally. PE is characterized by excessive release of damage-associated molecular patterns (DAMPs) into the maternal circulation. This DAMP-rich milieu acts on innate immune cells, inducing a proinflammatory state characterized by elevated cytokines such as IL-1β and IL-18.
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