Journal September 25, 2026 6 min read

What markers track exosomes?

Exosome tracking relies on a defined set of protein, RNA and lipid markers, from tetraspanins and ESCRT machinery to podocyte-specific proteins and microRNAs measured in urine and plasma.

peptides-pro Editorial

Exosomes are small extracellular vesicles of endosomal origin, formed when multivesicular bodies fuse with the plasma membrane and release their intraluminal vesicles into the extracellular space. They are tracked by a defined panel of markers: the tetraspanins CD9, CD63 and CD81, the endosomal sorting complexes required for transport (ESCRT) machinery, and, for functional studies, cargo-specific molecules such as microRNAs, metabolic proteins and tissue-restricted antigens. Identifiers vary by marker class rather than by a single formula; exosome preparations are typically characterised by particle size distribution, protein concentration and marker immunoreactivity rather than by a molecular weight or sequence.

The work described in the evidence below centres on several distinct pathways and receptor families, including epidermal growth factor receptor (EGFR) signalling in melanoma-keratinocyte crosstalk, AMPK/mTOR signalling in fibroblast glycolysis, and the TGF-β/SMAD and Hippo/TEAD1 axes in wound repair.

Research Studies

Podocyte-specific proteins and albuminuric diabetic kidney disease

A clinical study in African American Veterans with albuminuric stage 2 and 3 chronic diabetic kidney disease measured podocyte-specific injury markers in urinary exosomes, specifically nephrin, podocalyxin and Wilms' tumour protein (WT-1), in participants receiving empagliflozin, finerenone or combination therapy [1]. Secondary objectives correlated changes in exosome-based podocyte-specific proteins with standardised kidney injury biomarkers including urine albumin/creatinine ratio and estimated GFR, and with systemic inflammatory markers such as interleukins IL-1, IL-6 and IL-12, hs-CRP, and measures of arterial stiffness [1].

hsa-miR-221-5p and keratinocyte LL-37 in melanoma progression

In clinical specimens, cathelicidin LL-37 was spatially suppressed in tumour-adjacent epidermis relative to distal regions [2]. Melanoma-derived exosomes suppressed keratinocyte LL-37 expression, driven in part by exosomal hsa-miR-221-5p through impaired sustained EGFR signalling [2]. Keratinocyte-derived LL-37 curtailed melanoma cell migration, invasion and epithelial-mesenchymal transition, restrained tumour growth in vivo, and was associated with a tumour immune microenvironment enriched in M1 macrophages [2].

FGF21-modified ADSC exosomes and fibroblast glycolysis in wound healing

Adipose-derived mesenchymal stem cells overexpressing fibroblast growth factor 21 were established by genetic engineering, and FGF21-enriched exosomes (Exo@FGF21) were isolated and characterised by transmission electron microscopy and nanoparticle tracking analysis [3]. The study examined whether these engineered exosomes promote wound healing by activating fibroblast glycolysis through AMPK/mTOR signalling [3].

Cerebrolysin-treated endothelial cell exosomes and permeability

Using an in vitro endothelial permeability assay, a study tested whether exosomes released by Cerebrolysin-treated cerebral endothelial cells (Cerebro-Exos) act on dysfunctional cerebral endothelial cells [4]. Stoichiometric analysis showed marked differences in cargo profiles between Cerebro-Exos and exosomes from untreated cells (Naïve-Exos), with Cerebro-Exos highly enriched in metabolic and tight junction-related proteins [4]. Cerebro-Exos had a superior effect compared with Naïve-Exos on restoring cerebral endothelial cell integrity impaired by fibrin and tissue plasminogen activator [4].

Umbilical cord blood-derived stem cells and exosomes in autism spectrum disorder

A 12-month study tests whether AdiaVita, comprising umbilical cord blood-derived stem cells and exosomes, plus glutathione improves autism symptoms more than glutathione alone in children aged 3 to 12 [5]. Approximately 100 children with confirmed autism are randomly assigned to one of two groups; one receives monthly intravenous AdiaVita plus intravenous glutathione for 3 months, the other receives intravenous glutathione plus a saline placebo infusion for 2 months, and both groups use a topical glutathione spray twice daily at home [5]. Symptoms are tracked with the Autism Treatment Evaluation Checklist completed by a parent and by a therapist or teacher, with safety monitored at clinic visits through Month 12 [5].

Neuronal exosomes and brain-derived markers of exercise response

A study examining the brain-based biological mechanistic pathway by which exercise exerts anxiolytic effects measures brain-derived markers of mitochondrial metabolism (acetyl-L-carnitine) and inflammation (interleukin-6) using technology to isolate neuronal exosomes [7].

Wharton gel exosomes with autologous bone marrow cells in liver cirrhosis

A protocol in patients with liver cirrhosis, irrespective of stage and excluding those with active tumour or other major health issues endangering life, uses autologous bone marrow-derived mononuclear cells harvested from the same patient under local anaesthesia, followed by cell concentration and viability testing [8]. The final product is combined with a small volume of 2 cc of Wharton gel exosomes at 20 billion per dose and administered intravenously [8].

Regenerative approaches to craniofacial and corneal neuropathic pain

Craniofacial and corneal neuropathic pain are disabling conditions characterised by persistent pain frequently refractory to conventional pharmacologic and interventional therapies, arising from interactions between peripheral nerve injury, neuroinflammation and maladaptive central sensitisation within trigeminal pathways [6]. These features span neuropathic and nociplastic pain mechanisms as defined by the International Association for the Study of Pain, emphasising the need for mechanism-based, patient-stratified treatment strategies, and regenerative medicine offers a paradigm shift from symptom suppression toward structural nerve repair and functional restoration [6].

Comparison of exosome marker categories across the evidence

Marker category	Examples in the evidence	Specimen or model
Podocyte-specific proteins	Nephrin, podocalyxin, WT-1	Urine exosomes, African American Veterans with albuminuric stage 2–3 diabetic kidney disease [1]
Exosomal microRNA	hsa-miR-221-5p	Melanoma-derived exosomes acting on keratinocytes [2]
Metabolic and tight junction proteins	Metabolic and tight junction-related proteins	Cerebrolysin-treated cerebral endothelial cell exosomes, in vitro [4]
Brain-derived metabolic and inflammatory markers	Acetyl-L-carnitine, interleukin-6	Neuronal exosomes isolated after exercise [7]
Systemic inflammatory markers correlated with exosomal cargo	IL-1, IL-6, IL-12, hs-CRP	Serum, diabetic kidney disease cohort [1]

Additional mechanistic findings

Several further reports describe exosome-associated mechanisms without defining a single tracking marker. Cancer-associated fibroblast-derived exosomes delivering Snail were investigated for their regulation of the SOCS6/HIF-1α axis in pancreatic cancer stemness and gemcitabine resistance [9]. A chitosan hydrogel loaded with mesenchymal stem cell-derived exosomes accelerated wound closure and enhanced tissue regeneration in a full-thickness porcine skin defect model [10]. Combinatorial therapy with LL-37 and adipose-derived stem cells was studied for diabetic wound repair through NRROS-mediated crosstalk between the TGF-β/SMAD and Hippo/TEAD1 axes [11]. Surface-engineered GE11-functionalised exosomes were developed for EGFR-targeted peonidin delivery and suppression of SNAI1-mediated epithelial-mesenchymal transition in glioma [12].

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