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 (656 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
Supporting cells projecting inward from the basement membrane of seminiferous tubules. They surround and nourish the developing male germ cells and secrete the androgen-binding protein and hormones such as anti-mullerian hormone. The tight junctions of Sertoli cells with the spermatogonia and spermatocytes provide a blood-testis barrier.
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: Cells, Sertoli; Sertoli Cell; Cell, Sertoli.
Where it fits in the MeSH classification
- Broader topics
- Testis; Endocrine Cells; Epithelial Cells
Related concepts
- Seminiferous Tubules
- Androgen-Binding Protein
- Anti-Mullerian Hormone
- Spermatogonia
- Spermatocytes
- Blood-Testis Barrier
Research landscape
PubMed indexes 8,349 records tagged with the MeSH heading “Sertoli Cells” (counts retrieved 2026-10-31). 1,142 of them (13.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,544 records.
Reviews account for 677 records (8.1%) and meta-analyses for 4. Randomized controlled trials number 9 (0.1%) 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 | 3,544 |
| 2000-2009 | 1,804 |
| 2010-2019 | 1,859 |
| 2020 onward | 1,142 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 677 | 8.1% |
| Meta-analyses | 4 | 0.0% |
| Randomized controlled trials | 9 | 0.1% |
Method: PubMed query "Sertoli Cells"[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 |
|---|---|---|---|---|
| Single-cell analysis of developing and azoospermia human testicles reveals central role of Sertoli cells | 2020 | Research article Design not recorded in structured metadata | 238 | cc by PMID 33173058 · DOI · PMC7655944 |
| Multiple signaling pathways in Sertoli cells: recent findings in spermatogenesis | 2019 | Review article Design not recorded in structured metadata | 216 | cc by PMID 31316051 · DOI · PMC6637205 |
| The ACE2 expression in Sertoli cells and germ cells may cause male reproductive disorder after SARS-CoV-2 infection | 2020 | Research article Design not recorded in structured metadata | 136 | cc by PMID 32594644 · DOI · PMC7361928 |
| Glycogen and lactate metabolism in mouse fetal Sertoli cells sustain the germ line | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 41811847 · DOI · PMC13173509 |
Single-cell analysis of developing and azoospermia human testicles reveals central role of Sertoli cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Clinical efficacy of treatments against non-obstructive azoospermia (NOA), which affects 1% of men, are currently limited by the incomplete understanding of NOA pathogenesis and normal spermatogenic microenvironment.
- Closing excerpt
- We provide a novel perspective on the development of diagnostic methods and therapeutic targets for NOA.
- 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 (153 words)
Clinical efficacy of treatments against non-obstructive azoospermia (NOA), which affects 1% of men, are currently limited by the incomplete understanding of NOA pathogenesis and normal spermatogenic microenvironment. Here, we profile >80,000 human testicular single-cell transcriptomes from 10 healthy donors spanning the range from infant to adult and 7 NOA patients. We show that Sertoli cells, which form the scaffold in the testicular microenvironment, are severely damaged in NOA patients and identify the roadmap of Sertoli cell maturation. Notably, Sertoli cells of patients with congenital causes (Klinefelter syndrome and Y chromosome microdeletions) are mature, but exhibit abnormal immune responses, while the cells in idiopathic NOA (iNOA) are physiologically immature. Furthermore, we find that inhibition of Wnt signaling promotes the maturation of Sertoli cells from iNOA patients, allowing these cells to regain their ability to support germ cell survival. We provide a novel perspective on the development of diagnostic methods and therapeutic targets for NOA.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33173058 · DOI · PMC7655944
Multiple signaling pathways in Sertoli cells: recent findings in spermatogenesis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The functions of Sertoli cells in spermatogenesis have attracted much more attention recently.
- Closing excerpt
- Clarifying the mechanisms of signaling pathways in Sertoli cells on spermatogenesis provides new insights into the physiological functions of Sertoli cells in male reproduction, and also serves as a pre-requisite to identify potential therapeutic targets in abnormal spermatogenesis including testicular tumor and male infertility.
- 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 (193 words)
The functions of Sertoli cells in spermatogenesis have attracted much more attention recently. Normal spermatogenesis depends on Sertoli cells, mainly due to their influence on nutrient supply, maintenance of cell junctions, and support for germ cells' mitosis and meiosis. Accumulating evidence in the past decade has highlighted the dominant functions of the MAPK, AMPK, and TGF-β/Smad signaling pathways during spermatogenesis. Among these pathways, the MAPK signaling pathway regulates dynamics of tight junctions and adherens junctions, proliferation and meiosis of germ cells, proliferation and lactate production of Sertoli cells; the AMPK and the TGF-β/Smad signaling pathways both affect dynamics of tight junctions and adherens junctions, as well as the proliferation of Sertoli cells. The AMPK signaling pathway also regulates lactate supply. These signaling pathways combine to form a complex regulatory network for spermatogenesis. In testicular tumors or infertile patients, the activities of these signaling pathways in Sertoli cells are abnormal. Clarifying the mechanisms of signaling pathways in Sertoli cells on spermatogenesis provides new insights into the physiological functions of Sertoli cells in male reproduction, and also serves as a pre-requisite to identify potential therapeutic targets in abnormal spermatogenesis including testicular tumor and male infertility.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31316051 · DOI · PMC6637205
The ACE2 expression in Sertoli cells and germ cells may cause male reproductive disorder after SARS-CoV-2 infection [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The serious coronavirus disease-2019 (COVID-19) was first reported in December 2019 in Wuhan, China.
- Closing excerpt
- Taken together, this research provides a biological background of the potential route for infection of SARS-CoV-2 and may enable rapid deciphering male-related reproductive disorders induced by COVID-19.
- 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 (166 words)
The serious coronavirus disease-2019 (COVID-19) was first reported in December 2019 in Wuhan, China. COVID-19 is an infectious disease caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2). Angiotensin converting enzyme 2(ACE2) is the cellular receptor for SARS-CoV-2. Considering the critical roles of testicular cells for the transmission of genetic information between generations, we analyzed single-cell RNA-sequencing (scRNA-seq) data of adult human testis. The mRNA expression of ACE2 was expressed in both germ cells and somatic cells. Moreover, the positive rate of ACE2 in testes of infertile men was higher than normal, which indicates that SARS-CoV-2 may cause reproductive disorders through pathway activated by ACE2 and the men with reproductive disorder may easily to be infected by SARS-CoV-2. The expression level of ACE2 was related to the age, and the mid-aged with higher positive rate than young men testicular cells. Taken together, this research provides a biological background of the potential route for infection of SARS-CoV-2 and may enable rapid deciphering male-related reproductive disorders induced by COVID-19.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32594644 · DOI · PMC7361928
Glycogen and lactate metabolism in mouse fetal Sertoli cells sustain the germ line [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Metabolites are key regulators of cell fate decisions, chromatin remodeling, and lineage commitment.
- Closing excerpt
- These findings suggest that glycogen accumulation supports a critical developmental window in which both Sertoli and germ cells are metabolically constrained and unable to rely on external carbon sources.
- 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 (144 words)
Metabolites are key regulators of cell fate decisions, chromatin remodeling, and lineage commitment. While genetic pathways governing testis differentiation are well studied, the role of metabolism remains poorly understood. In this study, we investigate the transient, male-specific accumulation of glycogen in supporting cells of the fetal testis in mice, between embryonic days 11.5 and 13.5. Blocking glycogen metabolism/accumulation in vivo and in vitro is dispensable for Sertoli cell differentiation. However, its disruption leads to reduced lactate production and reduced germ cell number in the testis. Inhibiting lactate transport reveals a critical metabolic coupling between Sertoli and germ cells during early testis development. Surprisingly, external lactate or glucose supplementation fails to rescue the germ cell phenotype. These findings suggest that glycogen accumulation supports a critical developmental window in which both Sertoli and germ cells are metabolically constrained and unable to rely on external carbon sources.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41811847 · DOI · PMC13173509
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 Proliferation and functional maturation of Sertoli cells, and their relevance to disorders of testis function in adulthood [5]
- Research article Sertoli-Sertoli and Sertoli-germ cell interactions and their significance in germ cell movement in the seminiferous epithelium during spermatogenesis [6]
- Research article The central role of Sertoli cells in spermatogenesis [7]
- Research article Cell junction dynamics in the testis: Sertoli-germ cell interactions and male contraceptive development [8]
- Research article The Sertoli cell: one hundred fifty years of beauty and plasticity [9]
- Research article FSH and testosterone signaling in Sertoli cells [10]
References
- Zhao L, Yao C, Xing X, Jing T, Li P, Zhu Z, et al.. Single-cell analysis of developing and azoospermia human testicles reveals central role of Sertoli cells. . 2020. PMID 33173058 · DOI · PMC7655944
- Ni FD, Hao SL, Yang WX, Yang WX. Multiple signaling pathways in Sertoli cells: recent findings in spermatogenesis. . 2019. PMID 31316051 · DOI · PMC6637205
- Shen Q, Xiao X, Aierken A, Yue W, Wu X, Liao M, et al.. The ACE2 expression in Sertoli cells and germ cells may cause male reproductive disorder after SARS-CoV-2 infection. . 2020. PMID 32594644 · DOI · PMC7361928
- Estermann MA, Sheheen J, Grimm SA, Tezak B, Chen YY, Morita T, et al.. Glycogen and lactate metabolism in mouse fetal Sertoli cells sustain the germ line. . 2026. PMID 41811847 · DOI · PMC13173509
- Sharpe RM, McKinnell C, Kivlin C, Fisher JS. Proliferation and functional maturation of Sertoli cells, and their relevance to disorders of testis function in adulthood. Reproduction. 2003. PMID 12773099 · DOI
- Mruk DD, Cheng CY. Sertoli-Sertoli and Sertoli-germ cell interactions and their significance in germ cell movement in the seminiferous epithelium during spermatogenesis. Endocr Rev. 2004. PMID 15466940 · DOI
- Griswold MD. The central role of Sertoli cells in spermatogenesis. Semin Cell Dev Biol. 1998. PMID 9813187 · DOI
- Cheng CY, Mruk DD. Cell junction dynamics in the testis: Sertoli-germ cell interactions and male contraceptive development. Physiol Rev. 2002. PMID 12270945 · DOI
- França LR, Hess RA, Dufour JM, Hofmann MC, Griswold MD. The Sertoli cell: one hundred fifty years of beauty and plasticity. Andrology. 2016. PMID 26846984 · DOI · PMC5461925
- Walker WH, Cheng J. FSH and testosterone signaling in Sertoli cells. Reproduction. 2005. PMID 15985628 · 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.