Vimentin (VIM)
Overview
VIM encodes vimentin, a type III intermediate filament protein that is widely used as a marker of mesenchymal cell states. In normal biology, vimentin contributes to cytoskeletal organization, cell shape, mechanical resilience, migration, and intracellular scaffolding. Because of these functions, its expression is often associated with cells undergoing epithelial to mesenchymal transition (EMT), a process in which epithelial cells acquire more motile, invasive, and fibroblast-like properties.
In biomedical research, vimentin is frequently studied as both a phenotypic marker and a functional participant in disease processes. It is especially prominent in cancer biology, where increased vimentin expression is commonly linked to invasive behavior, metastatic potential, and partial EMT states. It is also investigated in non-malignant contexts, including renal injury and fibrotic remodeling, and in neuroinflammatory disease mechanisms where modified forms of vimentin may influence immune signaling.
Recent Publications Focus
2026-06-19 — Irbesartan and high-glucose-induced EMT in HK-2 cells.
This study examined epithelial-mesenchymal transition in HK-2 renal tubular epithelial cells under high-glucose conditions and assessed the effects of irbesartan. The authors measured mRNA and protein expression of NLRP3, caspase-1, NF-κB p65, α-SMA, vimentin, and N-cadherin by RT-qPCR and western blotting, linking VIM to an EMT/inflammatory phenotype in a setting involving the NLRP3 inflammasome and CASP1-related signaling 42318962Jun.2026-06-09 — Astrocytic PAD2, citrullinated vimentin, and amyloid pathology.
In an Immunity study focused on Alzheimer’s disease, PAD2 was shown to convert astrocytic vimentin into citrullinated vimentin (Cit-Vim175/184). This finding connects VIM to post-translational modification in astrocytes and suggests a mechanistic link between citrullinated vimentin, microglia activity, and exacerbation of amyloid pathology 41962542Apr.2026-05-27 — Primary carcinoma of the rete testis in a Nellore bull.
In this veterinary pathology report, neoplastic cells showed marked and diffuse immunostaining for vimentin and cytokeratin, while not staining for CD31. The result supports the use of vimentin as an immunohistochemical marker in tumor characterization and differential diagnosis 42201564May.2026-05-20 — Alginate-derived carbonized nanogels and tumor metastasis.
This study reported that Alg-CNGs attenuated metastasis in 4T1 triple-negative breast cancer cells by suppressing EMT. Specifically, the nanogels increased E-cadherin and decreased N-cadherin and vimentin, with reduced migration and invasion and disruption of actin organization and adhesion-related dynamics. These findings place VIM within a broader EMT program relevant to metastatic behavior 42167427May.2026-04-22 — Müller cell membrane biomimetic nanocarriers and VIM-mediated recognition.
This work described biomimetic nanocarriers that promoted efficient Ascl1 delivery through vimentin (VIM)-mediated specific cellular recognition. Here, VIM was used as a functional determinant of cell targeting, illustrating a non-canonical role for vimentin in nanocarrier-cell interactions and delivery specificity 42031060Apr.2026-04-17 — TMEM45B and liver cancer progression.
In a study of liver cancer progression, EMT-related changes were evaluated by immunofluorescence staining of vimentin and E-cadherin. VIM served as a readout of EMT status in the context of met signaling activation, reinforcing its role as a marker of phenotypic plasticity in cancer 41998230Apr.2026-03-30 — DNA self-assembly platform for lung cancer metastasis evaluation.
The constructed DNA-N@Ag+@PIX system employed vimentin as a marker in a biosensor-based strategy for evaluating lung cancer metastasis. This application highlights VIM’s utility in diagnostic and analytical platforms aimed at detecting metastatic phenotypes 41932242Apr.
What Changes, What Holds
1. Vimentin remains a readout of EMT even in inflammatory renal injury models
REINFORCES High-glucose HK-2 work keeps VIM in the established frame of epithelial-to-mesenchymal transition and phenotypic plasticity, now alongside NLRP3/CASP1-linked inflammatory signaling 42318962Jun. It does not displace the baseline account of vimentin as an EMT-associated marker and functional participant; instead, it sharpens the renal-injury context in which that association is being tracked.
2. Astrocytic vimentin can be post-translationally modified into a disease-linked form
NEW DIRECTION PAD2-driven citrullination adds a role not covered by the Overview: VIM is not just a mesenchymal marker or scaffolding protein here, but a substrate whose modified astrocytic form may influence microglia and amyloid pathology 41962542Apr. That extends the baseline into neurodegenerative mechanism, but it does not contradict the established EMT/cytoskeletal account.
3. Vimentin continues to serve as a diagnostic marker in tumor pathology
REINFORCES Diffuse immunostaining in a veterinary carcinoma mainly confirms the long-standing use of VIM in immunohistochemical tumor characterization and differential diagnosis 42201564May. The finding is specific to one neoplasm, but the class of claim is already well established in the Overview, so this adds an example rather than a new role.
4. Lower vimentin tracks reduced metastatic EMT behavior
REINFORCES Suppression of vimentin alongside restored epithelial markers fits the baseline view that VIM rises with invasive, mesenchymal-like cancer states 42167427May. The nanogel context is new, but the underlying claim is not: vimentin remains a marker and participant in metastatic EMT rather than a reversed or opposing signal.
5. Vimentin can be exploited as a cell-recognition handle for delivery systems
NEW DIRECTION Biomimetic nanocarrier targeting through VIM-mediated recognition adds a functional use not described in the Overview, which focuses on cytoskeletal, EMT, and disease-marker roles 42031060Apr. This does not overturn the baseline, but it does broaden vimentin from a state marker to a targeting determinant in engineered delivery.
6. Vimentin still indexes EMT status in liver cancer progression
REINFORCES Immunofluorescent vimentin readout in liver cancer simply extends the established cancer-biology use of VIM as a marker of phenotypic plasticity and invasive transition 41998230Apr. The met-linked context is additional detail, not a change in what vimentin is understood to signify.
7. Vimentin is being repurposed as a metastasis-detection signal in biosensor platforms
NEW DIRECTION Using VIM in a DNA-based analytical system adds a diagnostic engineering role that the Overview does not cover 41932242Apr. The baseline already supports vimentin as a marker of metastatic phenotypes, but this work shifts the emphasis toward assay design and detection rather than biology alone.
Overview update candidates: astrocytic PAD2-mediated citrullination of vimentin in Alzheimer’s-related pathology; vimentin-mediated cellular recognition for nanocarrier targeting; vimentin use in biosensor-based metastasis detection.
vim
Background Contexts
In the literature, the biological baseline, pathological conditions, or disease models commonly surrounding vim are described as follows:
- triple-negative (Other) — 2 papers: PMIDs 42013067, 41833656
- advanced lung cancer (Disease) — 1 paper: PMIDs 41932242
- Alzheimer's disease (Disease) — 1 paper: PMIDs 41962542
- antioxidant lipid nanoparticles (Technology) — 1 paper: PMIDs 42031060
- Carcinoma of the rete testis (Disease) — 1 paper: PMIDs 42201564
- diabetic nephropathy (Disease) — 1 paper: PMIDs 42318962
- epithelial to mesenchymal transition (Biological Process) — 1 paper: PMIDs 41998230
- esophageal squamous cell carcinoma (Disease) — 1 paper: PMIDs 42435533
- hyperglycemia (Biological Process) — 1 paper: PMIDs 42446820
- liver cancer (Disease) — 1 paper: PMIDs 41998230
- locally advanced gastric or gastroesophageal junction cancer (Disease) — 1 paper: PMIDs 42446820
- lung cancer metastasis (Disease) — 1 paper: PMIDs 41932242
Methodologies & Technologies Used
Researchers utilize the following experimental methods, imaging platforms, computational models, or biological reagents to study vim:
- CCK-8 assay (Technology) — 2 papers: PMIDs 42446820, 41998230
- epithelial to mesenchymal transition (Biological Process) — 2 papers: PMIDs 42443972, 42154344
- quantitative reverse transcription-PCR (Technology) — 2 papers: PMIDs 42435533, 42112999
- triple-negative breast adenocarcinoma (Cell Line) — 2 papers: PMIDs 42437425, 41833656
- 4T1 (Cell Line) — 1 paper: PMIDs 42437425
- 4T1 triple-negative breast cancer cells (Cell Line) — 1 paper: PMIDs 42167427
- 5×FAD mice (Organism) — 1 paper: PMIDs 41962542
- 680C91 (Therapy) — 1 paper: PMIDs 42112999
- [68Ga] DOTA-R01-MG (Therapy) — 1 paper: PMIDs 42426821
- AHNAK2 (Protein) — 1 paper: PMIDs 42443972
- alginate (Chemical) — 1 paper: PMIDs 42341146
- Anoctamin 1 (Protein) — 1 paper: PMIDs 42144424
Molecular Interventions & Targets
The primary molecular pathways, regulatory genes, enzymes, or therapeutic agents actively targeted and manipulated in relation to vim include:
- Cadherin 2 (Protein) — 2 papers: PMIDs 42318962, 42167427
- CDH1 (Protein) — 2 papers: PMIDs 42167427, 41998230
- Achaete-scute family bHLH transcription factor 1 (Gene) — 1 paper: PMIDs 42031060
- AKR1B1 (Gene) — 1 paper: PMIDs 42446820
- AKT serine/threonine kinase 1 (Protein) — 1 paper: PMIDs 41998230
- Anoctamin 1 (Protein) — 1 paper: PMIDs 42144424
- CAIX gene (Gene) — 1 paper: PMIDs 42013067
- Carbonic anhydrase 9 (Protein) — 1 paper: PMIDs 42013067
- CASP1 (Protein) — 1 paper: PMIDs 42318962
- CTHRC1 (Protein) — 1 paper: PMIDs 42435533
- cytokeratin (Protein) — 1 paper: PMIDs 42201564
- Daucosterol linoleate (Therapy) — 1 paper: PMIDs 42437425
Observed Outcomes & Phenotypes
The phenotypic changes, physiological endpoints, or clinical metrics observed and measured in connection with vim include:
- CDH1 (Protein) — 3 papers: PMIDs 42437425, 42144424, 42013067
- tumor cell proliferation (Clinical Metric) — 3 papers: PMIDs 42031060, 42013067, 41998230
- α-smooth muscle actin (Protein) — 3 papers: PMIDs 42435533, 42426821, 42112999
- Akt1 (Protein) — 2 papers: PMIDs 42167427, 42144424
- Cadherin 2 (Protein) — 2 papers: PMIDs 42437425, 42144424
- cdh-1 (Gene) — 2 papers: PMIDs 42446820, 42341146
- cdh-2 (Gene) — 2 papers: PMIDs 42446820, 42341146
- epithelial to mesenchymal transition (Biological Process) — 2 papers: PMIDs 42437425, 42435533
- matrix metalloproteinase-9 (Protein) — 2 papers: PMIDs 42435533, 42154344
- MMP2 (Protein) — 2 papers: PMIDs 42437425, 42154344
- snail (Protein) — 2 papers: PMIDs 42437425, 42144424
- (chemo)radiotherapy (Biological Process) — 1 paper: PMIDs 42013067
General Takeaways & Clinical Potentials
The high-level concepts, clinical translations, and overarching conclusions proposed in the research surrounding vim are summarized below:
- therapeutic target (Other) — 2 papers: PMIDs 42144424, 41962542
- 3D in vitro tumor models (Other) — 1 paper: PMIDs 42341146
- adjuvant therapeutic (Other) — 1 paper: PMIDs 42437425
- aggressive cancers (Disease) — 1 paper: PMIDs 41833656
- autophagy pathways (Biological Process) — 1 paper: PMIDs 41833656
- clinical PET studies (Other) — 1 paper: PMIDs 42426821
- clinically proximal models (Other) — 1 paper: PMIDs 42443972
- Cox Regression Analyses (Other) — 1 paper: PMIDs 41998230
- CTHRC1 (Protein) — 1 paper: PMIDs 42435533
- diabetic nephropathy (Disease) — 1 paper: PMIDs 42318962
- ECM remodeling pathways (Biological Process) — 1 paper: PMIDs 42435533
- fibrotic remodeling (Other) — 1 paper: PMIDs 42426821