Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (669 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A syndecan that interacts with extracellular matrix proteins and plays a role cell proliferation and cell migration.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Syndecan 1; CD138 Antigen; Antigen, CD138; Antigens, CD138; CD138 Antigens.
Where it fits in the MeSH classification
- Broader topics
- Syndecans
Related concepts
- Extracellular Matrix Proteins
- Cell Proliferation
- Cell Movement
Research landscape
PubMed indexes 2,193 records tagged with the MeSH heading “Syndecan-1” (counts retrieved 2026-10-31). 583 of them (26.6%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 914 records.
Reviews account for 102 records (4.7%) and meta-analyses for 14. Randomized controlled trials number 58 (2.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 101 |
| 2000-2009 | 595 |
| 2010-2019 | 914 |
| 2020 onward | 583 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 102 | 4.7% |
| Meta-analyses | 14 | 0.6% |
| Randomized controlled trials | 58 | 2.6% |
Method: PubMed query "Syndecan-1"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Modulation of syndecan-1 shedding after hemorrhagic shock and resuscitation | 2011 | Research article Design not recorded in structured metadata | 175 | cc by PMID 21886795 · DOI · PMC3158765 |
| Syndecan-1 in Cancer: Implications for Cell Signaling, Differentiation, and Prognostication | 2015 | Review article Design not recorded in structured metadata | 93 | cc by PMID 26420915 · DOI · PMC4569789 |
| Syndecan-1 is required to maintain intradermal fat and prevent cold stress | 2014 | Research article Design not recorded in structured metadata | 92 | cc by PMID 25101993 · DOI · PMC4125098 |
| Heparan Sulfates Regulate Vascular Reactivity in Syndecan 1 Knockout Mice | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 41683808 · DOI · PMC12897610 |
Modulation of syndecan-1 shedding after hemorrhagic shock and resuscitation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The early use of fresh frozen plasma as a resuscitative agent after hemorrhagic shock has been associated with improved survival, but the mechanism of protection is unknown.
- Closing excerpt
- These data suggest that plasma based resuscitation preserved endothelial syndecan-1 and maintained endothelial integrity, and may help to explain the protective effects of fresh frozen plasma after hemorrhagic shock.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (196 words)
The early use of fresh frozen plasma as a resuscitative agent after hemorrhagic shock has been associated with improved survival, but the mechanism of protection is unknown. Hemorrhagic shock causes endothelial cell dysfunction and we hypothesized that fresh frozen plasma would restore endothelial integrity and reduce syndecan-1 shedding after hemorrhagic shock. A prospective, observational study in severely injured patients in hemorrhagic shock demonstrated significantly elevated levels of syndecan-1 (554±93 ng/ml) after injury, which decreased with resuscitation (187±36 ng/ml) but was elevated compared to normal donors (27±1 ng/ml). Three pro-inflammatory cytokines, interferon-γ, fractalkine, and interleukin-1β, negatively correlated while one anti-inflammatory cytokine, IL-10, positively correlated with shed syndecan-1. These cytokines all play an important role in maintaining endothelial integrity. An in vitro model of endothelial injury then specifically examined endothelial permeability after treatment with fresh frozen plasma orlactated Ringers. Shock or endothelial injury disrupted junctional integrity and increased permeability, which was improved with fresh frozen plasma, but not lactated Ringers. Changes in endothelial cell permeability correlated with syndecan-1 shedding. These data suggest that plasma based resuscitation preserved endothelial syndecan-1 and maintained endothelial integrity, and may help to explain the protective effects of fresh frozen plasma after hemorrhagic shock.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 21886795 · DOI · PMC3158765
Syndecan-1 in Cancer: Implications for Cell Signaling, Differentiation, and Prognostication [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Syndecan-1, a cell surface heparan sulfate proteoglycan, is critically involved in the differentiation and prognosis of various tumors.
- Closing excerpt
- Moreover, we focus on the cellular localization of this proteoglycan as cell membrane anchored and/or shed, soluble syndecan-1 with stromal or nuclear accumulation and how this may carry different, highly tissue specific prognostic information for individual tumor types.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (95 words)
Syndecan-1, a cell surface heparan sulfate proteoglycan, is critically involved in the differentiation and prognosis of various tumors. In this review, we highlight the synthesis, cellular interactions, and the signalling pathways regulated by syndecan-1. The basal syndecan-1 level is also crucial for understanding the sequential changes involving malignant transformation, tumor progression, and advanced or disseminated cancer stages. Moreover, we focus on the cellular localization of this proteoglycan as cell membrane anchored and/or shed, soluble syndecan-1 with stromal or nuclear accumulation and how this may carry different, highly tissue specific prognostic information for individual tumor types.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26420915 · DOI · PMC4569789
Syndecan-1 is required to maintain intradermal fat and prevent cold stress [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Homeostatic temperature regulation is fundamental to mammalian physiology and is controlled by acute and chronic responses of local, endocrine and nervous regulators.
- Closing excerpt
- Our study indicates that disruption of intradermal adipose tissue development results in cold stress and complex metabolic pathology.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (188 words)
Homeostatic temperature regulation is fundamental to mammalian physiology and is controlled by acute and chronic responses of local, endocrine and nervous regulators. Here, we report that loss of the heparan sulfate proteoglycan, syndecan-1, causes a profoundly depleted intradermal fat layer, which provides crucial thermogenic insulation for mammals. Mice without syndecan-1 enter torpor upon fasting and show multiple indicators of cold stress, including activation of the stress checkpoint p38α in brown adipose tissue, liver and lung. The metabolic phenotype in mutant mice, including reduced liver glycogen, is rescued by housing at thermoneutrality, suggesting that reduced insulation in cool temperatures underlies the observed phenotypes. We find that syndecan-1, which functions as a facultative lipoprotein uptake receptor, is required for adipocyte differentiation in vitro. Intradermal fat shows highly dynamic differentiation, continuously expanding and involuting in response to hair cycle and ambient temperature. This physiology probably confers a unique role for Sdc1 in this adipocyte sub-type. The PPARγ agonist rosiglitazone rescues Sdc1-/- intradermal adipose tissue, placing PPARγ downstream of Sdc1 in triggering adipocyte differentiation. Our study indicates that disruption of intradermal adipose tissue development results in cold stress and complex metabolic pathology.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25101993 · DOI · PMC4125098
Heparan Sulfates Regulate Vascular Reactivity in Syndecan 1 Knockout Mice [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Heparan sulfates (HS) are polysaccharides abundantly expressed in the extracellular matrix and the glycocalyx of endothelial cells, having a putative role in vascular function.
- Closing excerpt
- Our data demonstrate a physiological role for HS in the regulation of the vascular tone in physiological conditions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (190 words)
Heparan sulfates (HS) are polysaccharides abundantly expressed in the extracellular matrix and the glycocalyx of endothelial cells, having a putative role in vascular function. The role of HS in vascular reactivity remains unclear. Herein, we sought to determine whether HS regulate the vascular tone in physiological conditions. Using male, 6-8-weeks-old, CD1, C57BL/6, syndecan 1 (Sdc1-/-) and glypican 1 (Gpc1-/-) knockout mice, we investigated if the degradation of HS with heparinase III altered vascular reactivity to norepinephrine (NE), acetylcholine (ACh) and potassium chloride (KCl). Our findings indicate that HS are crucial players in the vascular response to NE and ACh in CD1, C57BL/6, and Sdc1-/- but not in Gpc1-/- mice. Both Sdc1-/- and Gpc1-/- showed increased compensatory expression of syndecan 2 and syndecan 4. However, while Sdc1-/- showed decreased expression of glypican 1, Gpc1-/- showed increased expression of syndecan 1 in aortic homogenates. The lack of response to the vascular reactivity effects of heparinase III in Gpc1-/- suggests a differential role of HS to proteoglycan function in the regulation of the vascular tone. Our data demonstrate a physiological role for HS in the regulation of the vascular tone in physiological conditions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41683808 · DOI · PMC12897610
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Molecular functions of syndecan-1 in disease [5]
- Research article The heparanase/syndecan-1 axis in cancer: mechanisms and therapies [6]
- Research article Syndecan-1: a dynamic regulator of the myeloma microenvironment [7]
- Research article Synstatin: a selective inhibitor of the syndecan-1-coupled IGF1R-αvβ3 integrin complex in tumorigenesis and angiogenesis [8]
- Research article Endothelial Glycocalyx as Biomarker for Cardiovascular Diseases: Mechanistic and Clinical Implications [9]
- Research article Advances in the molecular functions of syndecan-1 (SDC1/CD138) in the pathogenesis of malignancies [10]
References
- Haywood-Watson RJ, Holcomb JB, Gonzalez EA, Peng Z, Pati S, Park PW, et al.. Modulation of syndecan-1 shedding after hemorrhagic shock and resuscitation. . 2011. PMID 21886795 · DOI · PMC3158765
- Szatmári T, Ötvös R, Hjerpe A, Dobra K. Syndecan-1 in Cancer: Implications for Cell Signaling, Differentiation, and Prognostication. . 2015. PMID 26420915 · DOI · PMC4569789
- Kasza I, Suh Y, Wollny D, Clark RJ, Roopra A, Colman RJ, et al.. Syndecan-1 is required to maintain intradermal fat and prevent cold stress. . 2014. PMID 25101993 · DOI · PMC4125098
- Potje SR, Katiki A, Pires PW, Chignalia AZ. Heparan Sulfates Regulate Vascular Reactivity in Syndecan 1 Knockout Mice. . 2026. PMID 41683808 · DOI · PMC12897610
- Teng YH, Aquino RS, Park PW. Molecular functions of syndecan-1 in disease. Matrix Biol. 2012. PMID 22033227 · DOI · PMC3568394
- Ramani VC, Purushothaman A, Stewart MD, Thompson CA, Vlodavsky I, Au JL, et al.. The heparanase/syndecan-1 axis in cancer: mechanisms and therapies. FEBS J. 2013. PMID 23374281 · DOI · PMC3651779
- Sanderson RD, Yang Y. Syndecan-1: a dynamic regulator of the myeloma microenvironment. Clin Exp Metastasis. 2008. PMID 18027090 · DOI · PMC3633534
- Rapraeger AC. Synstatin: a selective inhibitor of the syndecan-1-coupled IGF1R-αvβ3 integrin complex in tumorigenesis and angiogenesis. FEBS J. 2013. PMID 23375101 · DOI · PMC3651771
- Kim YH, Nijst P, Kiefer K, Tang WH. Endothelial Glycocalyx as Biomarker for Cardiovascular Diseases: Mechanistic and Clinical Implications. Curr Heart Fail Rep. 2017. PMID 28233259 · DOI · PMC5386320
- Gharbaran R. Advances in the molecular functions of syndecan-1 (SDC1/CD138) in the pathogenesis of malignancies. Crit Rev Oncol Hematol. 2015. PMID 25563413 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.