# Biomarkers of endothelial glycocalyx dysfunction in pregnancy: a systematic review of clinical relevance and detection techniques

**Authors:** Federica Fogacci, Duha Yahya, Jeanine Roeters Van Lennep, Katariina Öörni, Valentina Di Micoli, Francesco De Seta, Cristina Scollo, Claudio Borghi, Arrigo Francesco Giuseppe Cicero

PMC · DOI: 10.1007/s00011-026-02208-7 · Inflammation Research · 2026-03-17

## TL;DR

This review explores how changes in the endothelial glycocalyx during pregnancy are linked to complications like preeclampsia and how biomarkers could help detect these issues early.

## Contribution

The paper systematically reviews clinical relevance and detection techniques of endothelial glycocalyx biomarkers in pregnancy-related vascular disorders.

## Key findings

- Endothelial glycocalyx disruption is consistently associated with adverse maternal-fetal outcomes in pregnancy.
- Biomarkers like syndecan-1 and heparan sulfate show promise as non-invasive indicators of microvascular injury.
- Distinguishing early- from late-onset preeclampsia may benefit from glycocalyx-derived biomarkers.

## Abstract

The endothelial glycocalyx (EG) is a key regulator of vascular homeostasis, acting as a dynamic barrier between the bloodstream and the endothelium. In pregnancy, structural and functional alterations of the EG have been increasingly implicated in the pathogenesis of endothelial dysfunction, particularly in preeclampsia and other vascular complications. This systematic review critically examines current evidence on circulating biomarkers of EG degradation and their clinical relevance in hypertensive and metabolic disorders of pregnancy.

We explore the mechanistic role of the glycocalyx in maintaining vascular integrity, evaluate state-of-the-art detection methods—including sidestream dark field (SDF) imaging and biochemical assays—and summarize data on key circulating components such as syndecan-1, hyaluronic acid, heparan sulfate, and adhesion molecules.

Particular attention is given to distinguishing early- from late-onset preeclampsia and to other high-risk obstetric conditions, including gestational diabetes, fetal growth restriction, and infection-related complications. Despite heterogeneity across studies, most findings support a consistent association between EG disruption and adverse maternal–fetal outcomes.

This review highlights the potential of glycocalyx-derived biomarkers and imaging tools as non-invasive indicators of microvascular injury. Their integration into existing surveillance models could enhance early risk stratification and open new avenues for targeted clinical interventions in cardio-obstetric care.

The online version contains supplementary material available at 10.1007/s00011-026-02208-7.

## Linked entities

- **Proteins:** sdc1.L (syndecan 1 L homeolog)
- **Diseases:** preeclampsia (MONDO:0005081), gestational diabetes (MONDO:0005406), fetal growth restriction (MONDO:0005030)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, SELE (selectin E) [NCBI Gene 6401] {aka CD62E, ELAM, ELAM1, ESEL, LECAM2, selectin-e}, PGF (placental growth factor) [NCBI Gene 5228] {aka D12S1900, PGFL, PIGF, PLGF, PlGF-2, SHGC-10760}, HSPG2 (heparan sulfate proteoglycan 2) [NCBI Gene 3339] {aka HSPG, PLC, PRCAN, SJA, SJS, SJS1}, FLT1 (fms related receptor tyrosine kinase 1) [NCBI Gene 2321] {aka FLT, FLT-1, VEGFR-1, VEGFR1}, DCN (decorin) [NCBI Gene 1634] {aka CSCD, DSPG2, PG40, PGII, PGS2, SLRR1B}, HPSE (heparanase) [NCBI Gene 10855] {aka HPA, HPA1, HPR1, HPSE1, HSE1}, SDC1 (syndecan 1) [NCBI Gene 6382] {aka CD138, SDC, SYND1, syndecan}, SELP (selectin P) [NCBI Gene 6403] {aka CD62, CD62P, GMP140, GRMP, LECAM3, PADGEM}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, PODXL2 (podocalyxin like 2) [NCBI Gene 50512] {aka EG, PODLX2}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}, SDC2 (syndecan 2) [NCBI Gene 6383] {aka CD362, HSPG, HSPG1, SYND2}, PECAM1 (platelet and endothelial cell adhesion molecule 1) [NCBI Gene 5175] {aka CD31, CD31/EndoCAM, GPIIA', PECA1, PECAM-1, endoCAM}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}
- **Diseases:** EG injury (MESH:D057772), GH (MESH:D006432), HS (MESH:D009084), sepsis (MESH:D018805), bacteremia (MESH:D016470), preterm birth (MESH:D047928), chronic (MESH:D002908), infection (MESH:D007239), autoimmune disorders (MESH:D001327), trauma (MESH:D014947), metabolic disorders (MESH:D008659), end-organ damage (MESH:C564816), vascular dysfunction (MESH:D002561), inflammatory obstetric complications (MESH:D007744), Preeclampsia (MESH:D011225), vascular complications (MESH:D003925), maternal organ dysfunction (MESH:D009102), inflammation (MESH:D007249), GDM (MESH:D016640), Gestational Hypertension (MESH:D046110), endothelial dysfunction (MESH:D014652), preeclamptic (MESH:C538543), ischemia (MESH:D007511), placental dysfunction (MESH:D010922), CKD (MESH:D051436), diabetes (MESH:D003920), reperfusion injury (MESH:D015427), Acute Pyelonephritis (MESH:D011704), albuminuria (MESH:D000419), microvascular dysfunction (MESH:D017566), atherosclerosis (MESH:D050197), metabolic syndrome (MESH:D024821), EG (MESH:D005642), Chronic Hypertension (MESH:D006973), cardiovascular disease (MESH:D002318), placental abruption (MESH:D000037), complications (MESH:D008107), FGR (MESH:D005317)
- **Chemicals:** GAG (MESH:D006025), ruthenium red (MESH:D012430), nitric oxide (MESH:D009569), EG (-), heparinoids (MESH:D006496), Keratan Sulfate (MESH:D007632), HS (MESH:D006497), Dermatan Sulfate (MESH:D003871), KS (MESH:D011188), DS (MESH:D003903), HA (MESH:D006820), carbohydrate (MESH:D002241), CS (MESH:D002586), Chondroitin Sulfate (MESH:D002809)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12995992/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12995992/full.md

## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12995992/full.md

---
Source: https://tomesphere.com/paper/PMC12995992