EVOS M5000 Cardiovascular Microscope Review UK 2026
Curated literature review of peer-reviewed studies that used the EVOS M5000 Imaging System. Each paper is summarised by cell type, imaging technique, and disease area, with links to Google Scholar and PubMed. Plankton & Zoom does not host paywalled content.
Cardiovascular research often sits at the intersection of live-cell imaging, 3D hydrogel models, and long-term phenotype tracking. The EVOS M5000's on-stage incubation and easy-to-share image formats make it a practical choice for endothelial, smooth-muscle, and cardiomyocyte work.
Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead box M1 expression.
Cell type: Endothelial cells
Imaging technique: Fluorescence/senescence imaging
Disease area: Atherosclerosis / vascular aging
Cellular senescence of endothelial cells causes vascular dysfunction, promotes atherosclerosis, and contributes to the development of age-related vascular diseases. Sirtuin 6 (SIRT6), a conserved NAD+-dependent protein deacetylase, has beneficial effects against aging, despite th...
Aging (Albany NY) — PMID 33171439
Google Scholar | PubMed | DOI
Frequently asked questions about this study
What question does "Sirtuin 6 deficiency induces endothelial cell senescence via downregulation of forkhead..." answer? Cellular senescence of endothelial cells causes vascular dysfunction, promotes atherosclerosis, and contributes to the development of age-related vascular diseases. Sirtuin 6 (SIRT6), a conserved NAD+-dependent protein deacetylase, has beneficial effects against aging, despite th.
Why was the EVOS M5000 important for reaching this conclusion? EVOS M5000 fluorescence/senescence imaging supplied the visual evidence of endothelial senescence phenotypes, helping connect SIRT6 loss to the vascular ageing observations.
Dysfunction of iPSC-derived endothelial cells in human Hutchinson-Gilford progeria syndrome.
Cell type: iPSC-derived endothelial cells
Imaging technique: Brightfield/fluorescence imaging
Disease area: Hutchinson-Gilford progeria / cardiovascular aging
Children with Hutchinson-Gilford progeria syndrome (HGPS) succumb to myocardial infarction and stroke in their teen years. Endothelial dysfunction is an early event in more common forms of atherosclerosis. Endothelial pathobiology may contribute to HGPS, but a comprehensive chara...
Cell Cycle — PMID 31411525
Google Scholar | PubMed | DOI
Frequently asked questions about this study
What does this study conclude about Hutchinson-Gilford progeria / cardiovascular aging? Children with Hutchinson-Gilford progeria syndrome (HGPS) succumb to myocardial infarction and stroke in their teen years. Endothelial dysfunction is an early event in more common forms of atherosclerosis.
How did imaging on the EVOS M5000 support the finding? By combining brightfield overview images with fluorescence detail, the EVOS M5000 let the team document iPSC-derived endothelial morphology and marker expression in a single workflow.
Three-dimensional encapsulation of adult mouse cardiomyocytes in hydrogels with tunable stiffness.
Cell type: Adult mouse cardiomyocytes
Imaging technique: 3D hydrogel encapsulation, live-cell imaging
Disease area: Cardiovascular / heart disease
Numerous diseases, including those of the heart, are characterized by increased stiffness due to excessive deposition of extracellular matrix proteins. Cardiomyocytes continuously adapt their morphology and function to the mechanical changes of their microenvironment. Because tra...
Prog Biophys Mol Biol — PMID 31122749
Google Scholar | PubMed | DOI
Frequently asked questions about this study
What question does "Three-dimensional encapsulation of adult mouse cardiomyocytes in hydrogels with tunable..." answer? Numerous diseases, including those of the heart, are characterized by increased stiffness due to excessive deposition of extracellular matrix proteins. Cardiomyocytes continuously adapt their morphology and function to the mechanical changes of their microenvironment.
What role did the EVOS M5000 play in the result? The EVOS M5000 provided the live-cell imaging environment needed to track how adult mouse cardiomyocytes changed shape and behaviour inside hydrogels of different stiffness, linking mechanical cues to functional adaptation.
Endothelial cell-derived extracellular vesicles alter vascular smooth muscle cell phenotype through high-mobility group box proteins.
Cell type: Endothelial cells and vascular smooth muscle cells
Imaging technique: Exosome/vesicle imaging, fluorescence
Disease area: Cardiovascular disease
The vascular endothelium and smooth muscle form adjacent cellular layers that comprise part of the vascular wall. Each cell type can regulate the other's structure and function through a variety of paracrine effectors. Extracellular vesicles (EVs) are released from and transit be...
J Extracell Vesicles — PMID 32944170
Google Scholar | PubMed | DOI
Frequently asked questions about this study
What is the key finding of "Endothelial cell-derived extracellular vesicles alter vascular smooth muscle cell pheno..."? The vascular endothelium and smooth muscle form adjacent cellular layers that comprise part of the vascular wall. Each cell type can regulate the other's structure and function through a variety of paracrine effectors.
What did the EVOS M5000 contribute to the evidence? The EVOS M5000 was used to visualise extracellular vesicle labelling and the resulting changes in vascular smooth muscle cell phenotype, supporting the argument that endothelial vesicles carry paracrine signals.
STAT3-induced up-regulation of lncRNA NEAT1 as a ceRNA facilitates abdominal aortic aneurysm formation by elevating TULP3.
Cell type: Vascular smooth muscle cells / aortic tissue
Imaging technique: Live-cell / fluorescence imaging
Disease area: Abdominal aortic aneurysm
Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases. However, its function and mechanism in AAA were not precisely documented. Here, we explo...
Biosci Rep — PMID 31868202
Google Scholar | PubMed | DOI
Frequently asked questions about this study
What does this study conclude about Abdominal aortic aneurysm? Long noncoding RNAs (lncRNAs) were viewed as crucial participants in the pathogenesis of abdominal aortic aneurysm (AAA). LncRNA NEAT1 was recognized as an oncogenic gene in various diseases.
What did the EVOS M5000 contribute to the evidence? The EVOS M5000 was used for long-term live-cell and fluorescence imaging, letting the researchers follow vascular smooth muscle cells / aortic tissue behaviour over time in a stable on-stage environment.