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 (779 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 potent androgenic steroid and major product secreted by the leydig cells of the testis. Its production is stimulated by luteinizing hormone from the pituitary gland. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to dihydrotestosterone or estradiol.
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: 17-beta-Hydroxy-4-Androsten-3-one; 17 beta Hydroxy 4 Androsten 3 one; Testosterone Sulfate; Sustanon; 8-Isotestosterone; 8 Isotestosterone; 17-beta-Hydroxy-8 alpha-4-Androsten-3-one; 17 beta Hydroxy 8 alpha 4 Androsten 3 one.
Where it fits in the MeSH classification
- Broader topics
- Androstenols; Testosterone Congeners
- Narrower topics
- Epitestosterone; Hydroxytestosterones; Methenolone; Methyltestosterone; Testosterone Propionate
Related concepts
Research landscape
PubMed indexes 80,984 records tagged with the MeSH heading “Testosterone” (counts retrieved 2026-10-31). 9,957 of them (12.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 41,024 records.
Reviews account for 5,663 records (7.0%) and meta-analyses for 463. Randomized controlled trials number 2,633 (3.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 41,024 |
| 2000-2009 | 14,025 |
| 2010-2019 | 15,978 |
| 2020 onward | 9,957 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,663 | 7.0% |
| Meta-analyses | 463 | 0.6% |
| Randomized controlled trials | 2,633 | 3.3% |
Method: PubMed query "Testosterone"[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 |
|---|---|---|---|---|
| Luteinizing Hormone Regulates Testosterone Production, Leydig Cell Proliferation, Differentiation, and Circadian Rhythm During Spermatogenesis | 2025 | Review article Design not recorded in structured metadata | 45 | cc by PMID 40332028 · DOI · PMC12027374 |
| Testosterone affects female CD4+ T cells in healthy individuals and autoimmune liver diseases | 2025 | Research article Design not recorded in structured metadata | 17 | cc by PMID 40260919 · DOI · PMC12016935 |
| Unveiling mechanisms underlying kidney function changes during sex hormone therapy | 2025 | Research article Design not recorded in structured metadata | 16 | cc by PMID 40193283 · DOI · PMC12043095 |
| Understanding the Secular Decline in Testosterone: Mechanisms, Consequences, and Clinical Perspectives | 2026 | Review article Design not recorded in structured metadata | 5 | cc by PMID 41596342 · DOI · PMC12841019 |
Luteinizing Hormone Regulates Testosterone Production, Leydig Cell Proliferation, Differentiation, and Circadian Rhythm During Spermatogenesis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Male reproductive health, particularly the regulation of spermatogenesis, is controlled by a complex combination of factors, including luteinizing hormone (LH) and its effects on Leydig cells (LCs).
- Closing excerpt
- By highlighting key molecular mechanisms, this work provides insights into the therapeutic potential of LH in addressing male infertility and conditions of LC dysfunction.
- 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 (147 words)
Male reproductive health, particularly the regulation of spermatogenesis, is controlled by a complex combination of factors, including luteinizing hormone (LH) and its effects on Leydig cells (LCs). LH stimulates testosterone synthesis in LCs, which is critical for maintaining spermatogenesis and male fertility. This review examines the pathways through which LH regulates testosterone production, LC proliferation, differentiation, and circadian rhythm in human and non-human species. In particular, the signaling pathways of luteinizing hormone involved in testosterone production are discussed. Additionally, we explore LH's role in sperm maturation and quality, emphasizing its clinical implications in treating hypogonadotropic hypogonadism and diagnosing gonadal dysfunctions such as androgen insensitivity syndrome and precocious puberty. Furthermore, the potential of LH in assisted reproductive technologies for improving sperm quality is discussed. By highlighting key molecular mechanisms, this work provides insights into the therapeutic potential of LH in addressing male infertility and conditions of LC dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40332028 · DOI · PMC12027374
Testosterone affects female CD4+ T cells in healthy individuals and autoimmune liver diseases [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) are autoimmune liver diseases with strong female predominance.
- Closing excerpt
- We here report a direct effect of testosterone on CD4+ T cells that may contribute to future personalized treatment strategies.
- 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 (207 words)
Autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) are autoimmune liver diseases with strong female predominance. They are caused by T cell-mediated injury of hepatic parenchymal cells, but the mechanisms underlying this sex bias are unknown. Here, we investigated whether testosterone contributes to T cell activation in women with PBC. Compared with sex- and age-matched healthy controls (n = 23), cisgender (cis) women with PBC (n = 24) demonstrated decreased testosterone serum levels and proinflammatory CD4+ T cell profile in peripheral blood. Testosterone suppressed the expression of TNF and IFN-γ by human CD4+ T cells in vitro. In trans men receiving gender-affirming hormone therapy (GAHT) (n = 25), testosterone affected CD4+ T cell function by inhibiting Th1 and Th17 differentiation and by supporting the differentiation into regulatory Treg. Mechanistically, we provide evidence for a direct effect of testosterone on T cells using mice with T cell-specific deletion of the cytosolic androgen receptor. Supporting a role for testosterone in autoimmune liver disease, we observed an improved disease course and profound changes in T cell states in a trans man with AIH/primary sclerosing cholangitis (PSC) variant syndrome receiving GAHT. We here report a direct effect of testosterone on CD4+ T cells that may contribute to future personalized treatment strategies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40260919 · DOI · PMC12016935
Unveiling mechanisms underlying kidney function changes during sex hormone therapy [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BACKGROUNDMen with chronic kidney disease (CKD) experience faster kidney function decline than women.
- Closing excerpt
- gov (ID: NCT04482920).
- 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 (270 words)
BACKGROUNDMen with chronic kidney disease (CKD) experience faster kidney function decline than women. Studies in individuals undergoing sex hormone therapy suggest a role for sex hormones, as estimated glomerular filtration rate (eGFR) increases with feminizing therapy and decreases with masculinizing therapy. However, effects on measured GFR (mGFR), glomerular and tubular function, and involved molecular mechanisms remain unexplored.METHODSThis prospective, observational study included individuals initiating feminizing (estradiol and antiandrogens; n = 23) or masculinizing (testosterone; n = 21) therapy. Baseline and 3-month assessments included mGFR (iohexol clearance), kidney perfusion (para-aminohippuric acid clearance), tubular injury biomarkers, and plasma proteomics.RESULTSDuring feminizing therapy, mGFR and kidney perfusion increased (+3.6% and +9.1%, respectively; P < 0.05) without increased glomerular pressure. Tubular injury biomarkers, including urine neutrophil gelatinase-associated lipocalin, epidermal growth factor (EGF), monocyte chemoattractant protein-1, and chitinase 3-like protein 1 (YKL-40), decreased significantly (-53%, -42%, -45%, and -58%, respectively). During masculinizing therapy, mGFR and kidney perfusion remained unchanged, but urine YKL-40 and plasma tumor necrosis factor receptor 1 (TNFR-1) increased (+134% and +8%, respectively; P < 0.05). Proteomic analysis revealed differential expression of 49 proteins during feminizing and 356 proteins during masculinizing therapy. Many kidney-protective proteins were positively associated with estradiol and negatively associated with testosterone, including proteins involved in endothelial function (SFRP4, SOD3), inflammation reduction (TSG-6), and maintaining kidney tissue structure (agrin).CONCLUSIONSex hormones influence kidney physiology, with estradiol showing protective effects on glomerular and tubular function, while testosterone predominantly exerts opposing effects. These findings emphasize the role of sex hormones in sexual dimorphism observed in kidney function and physiology and suggest new approaches for sex-specific precision medicine.TRIAL REGISTRATIONDutch Trial Register (ID: NL9517); ClinicalTrials.gov (ID: NCT04482920).
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40193283 · DOI · PMC12043095
Understanding the Secular Decline in Testosterone: Mechanisms, Consequences, and Clinical Perspectives [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Testosterone is a key regulator of male and female physiology, influencing reproductive function, muscle and bone anabolism, metabolic homeostasis, and psychological well-being.
- Closing excerpt
- Overall, the contemporary testosterone decline represents a complex, multifactorial public health issue requiring integrated approaches to preserve hormonal and systemic health.
- 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 (155 words)
Testosterone is a key regulator of male and female physiology, influencing reproductive function, muscle and bone anabolism, metabolic homeostasis, and psychological well-being. Growing evidence indicates a secular, age-independent decline in testosterone levels across populations, a trend associated with reduced fertility, metabolic and cardiovascular dysfunction, mood disturbances, and impaired quality of life. While aging and genetic factors play a role, a wide range of modifiable influences-including obesity, physical inactivity, unhealthy dietary patterns, chronic stress, poor sleep, and exposure to endocrine-disrupting chemicals or other environmental stressors-appear to contribute substantially to this phenomenon. This narrative review synthesizes the evidence on testosterone's physiological significance, the causes and consequences of its secular decline, and evaluates potential interventions, emphasizing lifestyle and environmental strategies (physical activity, nutrition, weight management, sleep, stress reduction, sunlight exposure) as well as pharmacological and nutraceutical options. Overall, the contemporary testosterone decline represents a complex, multifactorial public health issue requiring integrated approaches to preserve hormonal and systemic health.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41596342 · DOI · PMC12841019
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 Clinical review 1: Adverse effects of testosterone therapy in adult men: a systematic review and meta-analysis [5]
- Research article Clinical review: Endogenous testosterone and mortality in men: a systematic review and meta-analysis [6]
- Research article Testosterone therapy and cardiovascular events among men: a systematic review and meta-analysis of placebo-controlled randomized trials [7]
- Research article Testosterone and cardiovascular risk in men: a systematic review and meta-analysis of randomized placebo-controlled trials [8]
- Research article Testosterone and metabolic syndrome: a meta-analysis study [9]
- Research article Testosterone and depression: systematic review and meta-analysis [10]
References
- Lei T, Yang Y, Yang WX. Luteinizing Hormone Regulates Testosterone Production, Leydig Cell Proliferation, Differentiation, and Circadian Rhythm During Spermatogenesis. . 2025. PMID 40332028 · DOI · PMC12027374
- Henze L, Will N, Lee D, Haas V, Casar C, Meyer J, et al.. Testosterone affects female CD4+ T cells in healthy individuals and autoimmune liver diseases. . 2025. PMID 40260919 · DOI · PMC12016935
- van Eeghen SA, Pyle L, Narongkiatikhun P, Choi YJ, Obeid W, Parikh CR, et al.. Unveiling mechanisms underlying kidney function changes during sex hormone therapy. . 2025. PMID 40193283 · DOI · PMC12043095
- Fraile-Martínez Ó, Ortega MA, García-Montero C. Understanding the Secular Decline in Testosterone: Mechanisms, Consequences, and Clinical Perspectives. . 2026. PMID 41596342 · DOI · PMC12841019
- Fernández-Balsells MM, Murad MH, Lane M, Lampropulos JF, Albuquerque F, Mullan RJ, et al.. Clinical review 1: Adverse effects of testosterone therapy in adult men: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2010. PMID 20525906 · DOI
- Araujo AB, Dixon JM, Suarez EA, Murad MH, Guey LT, Wittert GA. Clinical review: Endogenous testosterone and mortality in men: a systematic review and meta-analysis. J Clin Endocrinol Metab. 2011. PMID 21816776 · DOI · PMC3200249
- Xu L, Freeman G, Cowling BJ, Schooling CM. Testosterone therapy and cardiovascular events among men: a systematic review and meta-analysis of placebo-controlled randomized trials. BMC Med. 2013. PMID 23597181 · DOI · PMC3648456
- Haddad RM, Kennedy CC, Caples SM, Tracz MJ, Boloña ER, Sideras K, et al.. Testosterone and cardiovascular risk in men: a systematic review and meta-analysis of randomized placebo-controlled trials. Mayo Clin Proc. 2007. PMID 17285783 · DOI
- Corona G, Monami M, Rastrelli G, Aversa A, Tishova Y, Saad F, et al.. Testosterone and metabolic syndrome: a meta-analysis study. J Sex Med. 2011. PMID 20807333 · DOI
- Zarrouf FA, Artz S, Griffith J, Sirbu C, Kommor M. Testosterone and depression: systematic review and meta-analysis. J Psychiatr Pract. 2009. PMID 19625884 · 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.