Restenosis is a pathophysiological phenomenon that can occur in patients submitted to revascularization procedures (bypass, endarterectomy, angioplasty), possibly resulting in new narrowing of injured vessels. Vascular restenosis remains a pressing clinical problem, despite the therapeutic strategies and devices developed so far. Stem cells hold a great potential for the regeneration of damaged tissues in cardiovascular diseases. Recent studies clearly indicated that different stem cell populations contribute to vascular remodeling after injury. Nevertheless, the exact role of vascular cell precursors in restenosis pathophysiology is not yet well defined, as heterogeneous and contrasting data are currently available. Mesenchymal stromal/stem cells (MSCs) are non-hematopoietic multi-potent stem-like cells able of differentiating into both mesenchymal and non-mesenchymal lineages. MSCs offer a series of advantages: a) they can be isolated from a small aspirate of bone marrow; b) extensively proliferate in vitro while preserving a normal karyotype and telomerase activity on several passages; c) express low immunogenicity and hence their use should not require a pharmacological immunosuppression. MSCs have an intrinsic ability to differentiate into functional cell types able to repair the diseased or injured tissue in which they are localised. For this reason, MSCs are currently under scrutiny for treatment of different cardiovascular diseases. Nevertheless, it has not yet been clearly determined whether MSCs can substantially contribute to a positive resolution of restenosis after vascular injury. This review will provide information about the mechanisms at the basis of vascular restenosis and the current knowledge of the role, positive or negative, played by MSCs in restenosis progression as highlighted by recent experimental protocols.
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http://dx.doi.org/10.2174/157016109788340776 | DOI Listing |
Blood Adv
January 2025
Department of Hematology, Oncology, Hemostaseology, and Stem Cell Transplantation, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Interferon alpha (IFNa) is approved for the therapy of patients (pts) with polycythemia vera (PV), a subtype of myeloproliferative neoplasms (MPN). Some pts achieve molecular responses (MR), but clonal factors sensitizing for MR remain elusive. We integrated colony formation and differentiation assays with single-cell RNA seq and genotyping in PV-derived cells vs.
View Article and Find Full Text PDFBlood Adv
January 2025
Univeristy of Alabama at Birmingham, Birmingham, Alabama, United States.
Hepatosplenic T-cell lymphoma (HSTCL) is an aggressive mature T-cell lymphoma characterized by significant hepatosplenomegaly, bone marrow involvement, and minimal or no lymphadenopathy. Primarily affecting young adults, it is exceptionally rare in children and adolescents. This makes diagnosis and treatment particularly challenging for pathologists and pediatric oncologists.
View Article and Find Full Text PDFPLoS Biol
January 2025
Cardiovascular Institute and Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Definitive hematopoietic stem and progenitor cells (HSPCs) arise from a small number of hemogenic endothelial cells (HECs) within the developing embryo. Understanding the origin and ontogeny of HSPCs is of considerable interest and potential therapeutic value. It has been proposed that the murine placenta contains HECs that differentiate into HSPCs.
View Article and Find Full Text PDFPLoS One
January 2025
Division of Pharmacology, Department of Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands.
Toll-like receptor (TLRs) activation in multiple myeloma (MM) cells induces heterogeneous functional responses including cell growth and proliferation, survival or apoptosis. These effects have been suggested to be partly due to increase in secretion of cytokines such as IL-6 or IFNα among others from MM cells following TLR activation. However, whether triggering of these receptors also modulates production of immunoglobulin free light chains (FLCs), which largely contribute to MM pathology, has not been investigated in MM cells before.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Center for Medical Research and Innovation, Shanghai Pudong Hospital, Institutes of Biomedical Sciences, Chinese Academy of Medical Sciences (RU069), Medical College of Fudan University, Shanghai 201399, China.
Ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine (mC) in DNA, contributing to the regulation of gene transcription. Diverse mutations of TET2 are frequently found in various blood cancers, yet the full scope of their functional consequences has been unexplored. Here, we report that a subset of TET2 mutations identified in leukemia patients alter the substrate specificity of TET2 from acting on mC to thymine.
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