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 (741 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 darkly stained mat-like extracellular matrix (ECM) that separates cell layers, such as epithelium from endothelium or a layer of connective tissue. The ECM layer that supports an overlying epithelium or endothelium is called basal lamina. Basement membrane (BM) can be formed by the fusion of either two adjacent basal laminae or a basal lamina with an adjacent reticular lamina of connective tissue. BM, composed mainly of TYPE IV collagen; glycoprotein laminin; and proteoglycan, provides barriers as well as channels between interacting cell layers.
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: Basement Membranes; Membrane, Basement; Membranes, Basement; Basal Lamina; Lamina, Basal; Basement Lamina; Lamina, Basement; Lamina Lucida.
Where it fits in the MeSH classification
- Broader topics
- Membranes; Extracellular Matrix
- Narrower topics
- Basilar Membrane; Bruch Membrane; Descemet Membrane; Glomerular Basement Membrane
Related concepts
- Extracellular Matrix
- Epithelium
- Endothelium
- Connective Tissue
- Collagen
- Laminin
- Proteoglycans
Research landscape
PubMed indexes 27,022 records tagged with the MeSH heading “Basement Membrane” (counts retrieved 2026-10-31). 2,471 of them (9.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 15,918 records.
Reviews account for 2,491 records (9.2%) and meta-analyses for 60. Randomized controlled trials number 146 (0.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 15,918 |
| 2000-2009 | 4,407 |
| 2010-2019 | 4,226 |
| 2020 onward | 2,471 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 2,491 | 9.2% |
| Meta-analyses | 60 | 0.2% |
| Randomized controlled trials | 146 | 0.5% |
Method: PubMed query "Basement Membrane"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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 |
|---|---|---|---|---|
| The Human Epidermal Basement Membrane: A Shaped and Cell Instructive Platform That Aging Slowly Alters | 2020 | Review article Design not recorded in structured metadata | 113 | cc by PMID 33260936 · DOI · PMC7760980 |
| Basement membrane collagens and disease mechanisms | 2019 | Review article Design not recorded in structured metadata | 98 | cc by PMID 31387942 · DOI · PMC6744580 |
| Three-dimensional tonotopic mapping of the human cochlea based on synchrotron radiation phase-contrast imaging | 2021 | Research article Design not recorded in structured metadata | 77 | cc by PMID 33627724 · DOI · PMC7904830 |
| Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42378035 · DOI · PMC13574157 |
The Human Epidermal Basement Membrane: A Shaped and Cell Instructive Platform That Aging Slowly Alters [1]
Abstract reading summary — source excerpts
- Opening excerpt
- One of the most important functions of skin is to act as a protective barrier.
- Closing excerpt
- This review combines recent and older data on organization of the dermal-epidermal junction, its mechanical properties and role in mechanotransduction, its involvement in regeneration, and its fate during the aging process.
- 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 (201 words)
One of the most important functions of skin is to act as a protective barrier. To fulfill this role, the structural integrity of the skin depends on the dermal-epidermal junction-a complex network of extracellular matrix macromolecules that connect the outer epidermal layer to the underlying dermis. This junction provides both a structural support to keratinocytes and a specific niche that mediates signals influencing their behavior. It displays a distinctive microarchitecture characterized by an undulating pattern, strengthening dermal-epidermal connectivity and crosstalk. The optimal stiffness arising from the overall molecular organization, together with characteristic anchoring complexes, keeps the dermis and epidermis layers extremely well connected and capable of proper epidermal renewal and regeneration. Due to intrinsic and extrinsic factors, a large number of structural and biological changes accompany skin aging. These changes progressively weaken the dermal-epidermal junction substructure and affect its functions, contributing to the gradual decline in overall skin physiology. Most changes involve reduced turnover or altered enzymatic or non-enzymatic post-translational modifications, compromising the mechanical properties of matrix components and cells. This review combines recent and older data on organization of the dermal-epidermal junction, its mechanical properties and role in mechanotransduction, its involvement in regeneration, and its fate during the aging process.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33260936 · DOI · PMC7760980
Basement membrane collagens and disease mechanisms [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Basement membranes (BMs) are specialised extracellular matrix (ECM) structures and collagens are a key component required for BM function.
- Closing excerpt
- The identification of pathomolecular mechanisms of collagen mutations shared between different disorders represent an attractive prospect for treatments that may be effective across phenotypically distinct disorders.
- 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 (161 words)
Basement membranes (BMs) are specialised extracellular matrix (ECM) structures and collagens are a key component required for BM function. While collagen IV is the major BM collagen, collagens VI, VII, XV, XVII and XVIII are also present. Mutations in these collagens cause rare multi-systemic diseases but these collagens have also been associated with major common diseases including stroke. Developing treatments for these conditions will require a collective effort to increase our fundamental understanding of the biology of these collagens and the mechanisms by which mutations therein cause disease. Novel insights into pathomolecular disease mechanisms and cellular responses to these mutations has been exploited to develop proof-of-concept treatment strategies in animal models. Combined, these studies have also highlighted the complexity of the disease mechanisms and the need to obtain a more complete understanding of these mechanisms. The identification of pathomolecular mechanisms of collagen mutations shared between different disorders represent an attractive prospect for treatments that may be effective across phenotypically distinct disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31387942 · DOI · PMC6744580
Three-dimensional tonotopic mapping of the human cochlea based on synchrotron radiation phase-contrast imaging [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The human cochlea transforms sound waves into electrical signals in the acoustic nerve fibers with high acuity.
- Closing excerpt
- The three-dimensional tonotopic data presented herein has large implications for validating electrode position and creating customized frequency maps for cochlear implant recipients.
- 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 (178 words)
The human cochlea transforms sound waves into electrical signals in the acoustic nerve fibers with high acuity. This transformation occurs via vibrating anisotropic membranes (basilar and tectorial membranes) and frequency-specific hair cell receptors. Frequency-positions can be mapped within the cochlea to create a tonotopic chart which fits an almost-exponential function with lowest frequencies positioned apically and highest frequencies positioned at the cochlear base (Bekesy 1960, Greenwood 1961). To date, models of frequency positions have been based on a two-dimensional analysis with inaccurate representations of the cochlear hook region. In the present study, the first three-dimensional frequency analysis of the cochlea using dendritic mapping to obtain accurate tonotopic maps of the human basilar membrane/organ of Corti and the spiral ganglion was performed. A novel imaging technique, synchrotron radiation phase-contrast imaging, was used and a spiral ganglion frequency function was estimated by nonlinear least squares fitting a Greenwood-like function (F = A (10ax - K)) to the data. The three-dimensional tonotopic data presented herein has large implications for validating electrode position and creating customized frequency maps for cochlear implant recipients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33627724 · DOI · PMC7904830
Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Autosomal dominant polycystic kidney disease (ADPKD), the leading genetic cause of kidney failure, results from loss-of-function mutations in PKD1, encoding polycystin-1 (PC1).
- Closing excerpt
- Together, these findings establish a TBM-centered biomechanical model of ADPKD in which tubule deformation is governed by both basolateral and luminal mechanical factors and identify the cilium/TBM axis, operating in part through GLIS2, as a central driver of cystogenesis.
- 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 (201 words)
Autosomal dominant polycystic kidney disease (ADPKD), the leading genetic cause of kidney failure, results from loss-of-function mutations in PKD1, encoding polycystin-1 (PC1). PC1 localizes to the primary cilium. In the absence of PC1, adverse signaling from the primary cilium orchestrates cyst formation, but the biomechanical underpinnings of this cilia-dependent cyst activation (CDCA) remain unclear. Combining tubule-specific orthologous mouse models with a tubule-on-chip platform, we show that PC1 and cilia govern the composition, mechanical properties, and shape of the tubular basement membrane (TBM), the principal rigid determinant of tubule geometry. PC1 loss triggered TBM thinning, heparan sulfate enrichment, and deformation, leading to distension, preferentially of the distal nephron. These changes were driven by a cilia-dependent transcriptional program, with GLIS2 - a key CDCA effector - participating as a downstream mediator. Reduction of TBM stiffness amplified Pkd1-/- tubule-on-chip dilation and increased cyst formation in vivo. Conversely, increasing luminal pressure through ureteral obstruction induced disproportionate distension of Pkd1-deficient tubules and triggered an irreversible cystogenic program. Together, these findings establish a TBM-centered biomechanical model of ADPKD in which tubule deformation is governed by both basolateral and luminal mechanical factors and identify the cilium/TBM axis, operating in part through GLIS2, as a central driver of cystogenesis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42378035 · DOI · PMC13574157
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 Matrigel: basement membrane matrix with biological activity [5]
- Research article Basement membranes: cell scaffoldings and signaling platforms [6]
- Research article Laminin and other basement membrane components [7]
- Research article Podocyte injury and its consequences [8]
- Research article The nature and biology of basement membranes [9]
- Research article The vascular basement membrane in the healthy and pathological brain [10]
References
- Roig-Rosello E, Rousselle P. The Human Epidermal Basement Membrane: A Shaped and Cell Instructive Platform That Aging Slowly Alters. . 2020. PMID 33260936 · DOI · PMC7760980
- Gatseva A, Sin YY, Brezzo G, Van Agtmael T. Basement membrane collagens and disease mechanisms. . 2019. PMID 31387942 · DOI · PMC6744580
- Li H, Helpard L, Ekeroot J, Rohani SA, Zhu N, Rask-Andersen H, et al.. Three-dimensional tonotopic mapping of the human cochlea based on synchrotron radiation phase-contrast imaging. . 2021. PMID 33627724 · DOI · PMC7904830
- Mazloum M, Lapin B, Alghamdi R, Vandensteen J, Burtin M, Houillier P, et al.. Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease. . 2026. PMID 42378035 · DOI · PMC13574157
- Kleinman HK, Martin GR. Matrigel: basement membrane matrix with biological activity. Semin Cancer Biol. 2005. PMID 15975825 · DOI
- Yurchenco PD. Basement membranes: cell scaffoldings and signaling platforms. Cold Spring Harb Perspect Biol. 2011. PMID 21421915 · DOI · PMC3039528
- Martin GR, Timpl R. Laminin and other basement membrane components. Annu Rev Cell Biol. 1987. PMID 3318883 · DOI
- Nagata M. Podocyte injury and its consequences. Kidney Int. 2016. PMID 27165817 · DOI
- Pozzi A, Yurchenco PD, Iozzo RV. The nature and biology of basement membranes. Matrix Biol. 2017. PMID 28040522 · DOI · PMC5387862
- Thomsen MS, Routhe LJ, Moos T. The vascular basement membrane in the healthy and pathological brain. J Cereb Blood Flow Metab. 2017. PMID 28753105 · DOI · PMC5624399
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.