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 (746 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
An antagonist of angiotensin type 1 receptor with antihypertensive activity due to the reduced pressor effect of angiotensin II.
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: 2-Butyl-4-chloro-1-((2'-(1H-etrazol-5-yl) (1,1'-biphenyl)-4-yl)methyl)-1H-imidazole-5-methanol; DuP-753; DuP753; DuP 753; MK-954; MK 954; MK954; Losartan Potassium.
Where it fits in the MeSH classification
- Broader topics
- Biphenyl Compounds; Imidazoles; Tetrazoles
- See also
- Valsartan
Related concepts
- Angiotensin Type
- Receptor
- Angiotensin
Research landscape
PubMed indexes 7,501 records tagged with the MeSH heading “Losartan” (counts retrieved 2026-10-31). 768 of them (10.2%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 2,887 records.
Reviews account for 471 records (6.3%) and meta-analyses for 36. Randomized controlled trials number 1,018 (13.6%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,845 |
| 2000-2009 | 2,887 |
| 2010-2019 | 2,001 |
| 2020 onward | 768 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 471 | 6.3% |
| Meta-analyses | 36 | 0.5% |
| Randomized controlled trials | 1,018 | 13.6% |
Method: PubMed query "Losartan"[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 |
|---|---|---|---|---|
| Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury | 2014 | Research article Design not recorded in structured metadata | 224 | cc by PMID 25391767 · DOI · PMC4229671 |
| Losartan ameliorates dystrophic epidermolysis bullosa and uncovers new disease mechanisms | 2015 | Research article Design not recorded in structured metadata | 154 | cc by PMID 26194911 · DOI · PMC4568953 |
| Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70 | 2021 | Review article Design not recorded in structured metadata | 76 | cc by PMID 34831368 · DOI · PMC8619557 |
| Losartan and prednisolone for post-COVID syndrome and cardiac inflammation: a randomized, double-blind, placebo-controlled trial | 2026 | Randomized controlled trial Design not recorded in structured metadata | 0 | cc by PMID 42533000 · DOI · PMC13424660 |
Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Since March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China.
- Closing excerpt
- The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks.
- 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 (167 words)
Since March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China. Although most infections resulted in respiratory illness, some severe cases resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that further contributes to morbidity. To date, no effective drugs that improve the clinical outcome of influenza A (H7N9) virus-infected patients have been identified. Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease, and acute lung injury. In the current study, we report that ACE2 could mediate the severe acute lung injury induced by influenza A (H7N9) virus infection in an experimental mouse model. Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25391767 · DOI · PMC4229671
Losartan ameliorates dystrophic epidermolysis bullosa and uncovers new disease mechanisms [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Genetic loss of collagen VII causes recessive dystrophic epidermolysis bullosa (RDEB)-a severe skin fragility disorder associated with lifelong blistering and disabling progressive soft tissue fibrosis.
- Closing excerpt
- Inhibition of TGF-β activity limits these unwanted outcomes and thereby substantially ameliorates long-term symptoms.
- 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 (169 words)
Genetic loss of collagen VII causes recessive dystrophic epidermolysis bullosa (RDEB)-a severe skin fragility disorder associated with lifelong blistering and disabling progressive soft tissue fibrosis. Causative therapies for this complex disorder face major hurdles, and clinical implementation remains elusive. Here, we report an alternative evidence-based approach to ameliorate fibrosis and relieve symptoms in RDEB. Based on the findings that TGF-β activity is elevated in injured RDEB skin, we targeted TGF-β activity with losartan in a preclinical setting. Long-term treatment of RDEB mice efficiently reduced TGF-β signaling in chronically injured forepaws and halted fibrosis and subsequent fusion of the digits. In addition, proteomics analysis of losartan- vs. vehicle-treated RDEB skin uncovered changes in multiple proteins related to tissue inflammation. In line with this, losartan reduced inflammation and diminished TNF-α and IL-6 expression in injured forepaws. Collectively, the data argue that RDEB fibrosis is a consequence of a cascade encompassing tissue damage, TGF-β-mediated inflammation, and matrix remodeling. Inhibition of TGF-β activity limits these unwanted outcomes and thereby substantially ameliorates long-term symptoms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26194911 · DOI · PMC4568953
Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease after diabetes.
- Closing excerpt
- The role of the Hsp70 chaperone on the angiotensin II-induced EMT after angiotensin II type 1 receptor (AT1R) blockage, as a possible molecular target for therapeutic strategy against hypertensive renal damage is discussed.
- 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 (173 words)
Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease after diabetes. For years, hypertensive kidney disease has been focused on the afferent arterioles and glomeruli damage and the involvement of the renin angiotensin system (RAS). Nonetheless, in recent years, novel evidence has demonstrated that persistent high blood pressure injures tubular cells, leading to epithelial-mesenchymal transition (EMT) and tubulointerstitial fibrosis. Injury primarily determined at the glomerular level by hypertension causes changes in post-glomerular peritubular capillaries that in turn induce endothelial damage and hypoxia. Microvasculature dysfunction, by inducing hypoxic environment, triggers inflammation, EMT with epithelial cells dedifferentiation and fibrosis. Hypertensive kidney disease also includes podocyte effacement and loss, leading to disruption of the filtration barrier. This review highlights the molecular mechanisms and histologic aspects involved in the pathophysiology of hypertensive kidney disease incorporating knowledge about EMT and tubulointerstitial fibrosis. The role of the Hsp70 chaperone on the angiotensin II-induced EMT after angiotensin II type 1 receptor (AT1R) blockage, as a possible molecular target for therapeutic strategy against hypertensive renal damage is discussed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34831368 · DOI · PMC8619557
Losartan and prednisolone for post-COVID syndrome and cardiac inflammation: a randomized, double-blind, placebo-controlled trial [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Persistent cardiac symptoms are common in post-COVID syndrome, even without structural heart disease.
- Closing excerpt
- Trial registration: EudraCT 2022-001682-12; NCT05619653.
- 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 (237 words)
Persistent cardiac symptoms are common in post-COVID syndrome, even without structural heart disease. Evidence implicates immune dysregulation, endothelial dysfunction and low-grade cardiovascular inflammation. Yet no targeted treatment exists. Myoflame-19 is a multicenter, double-blind clinical trial of 279 participants with inflammatory cardiac involvement defined by cardiovascular magnetic resonance, randomized 1:1 to losartan plus prednisolone (n = 139) or matching placebos (n = 140) for 16 weeks. The modified intention-to-treat population comprised 124 and 122 participants. The primary endpoint, change in left ventricular (LV) ejection fraction, was neutral: between-group difference 0.74 percentage points (pp), 95%CI -0.14 to 1.62, p = 0.10, unpaired t-test; supportive baseline-adjusted ANCOVA 0.99, 95%CI 0.15-1.83, p = 0.021. Among prespecified secondary endpoints, several symptom and imaging measures showed numerical differences favoring intervention, including Average Symptom Score components (modified Canadian Chest Pain Scale -4.8 pp, 95%CI -17.3 to 7.6; NYHA class -8.1 pp, -20.6 to 4.3; Long COVID symptom burden -7.7 pp, -18.9 to 3.6), native T1 and T2 values (native T1 -2.46 ms, -8.35 to 3.42; native T2 -0.31 ms, -1.16 to 0.53), and LV end-diastolic volume ( + 1.45 ml/m², -0.09 to 3.00); however, confidence intervals included the null value and these findings should be regarded as hypothesis-generating.Treatment was safe and well-tolerated. These findings indicate a neutral treatment effect on the primary endpoint. They inform targeted immunomodulation and design of future trials in post-COVID syndrome and inflammatory cardiac involvement. Trial registration: EudraCT 2022-001682-12; NCT05619653.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42533000 · DOI · PMC13424660
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 pharmacokinetics of losartan [5]
- Research article Uric acid: role in cardiovascular disease and effects of losartan [6]
- Research article Angiotensin II antagonists for hypertension: are there differences in efficacy? [7]
- Research article Angiotensin II receptor blockers in patients with ACE inhibitor-induced angioedema [8]
- Research article Recent advances in understanding Marfan syndrome: should we now treat surgical patients with losartan? [9]
- Research article Losartan, an orally active angiotensin (AT1) receptor antagonist: a review of its efficacy and safety in essential hypertension [10]
References
- Yang P, Gu H, Zhao Z, Wang W, Cao B, Lai C, et al.. Angiotensin-converting enzyme 2 (ACE2) mediates influenza H7N9 virus-induced acute lung injury. . 2014. PMID 25391767 · DOI · PMC4229671
- Nyström A, Thriene K, Mittapalli V, Kern JS, Kiritsi D, Dengjel J, et al.. Losartan ameliorates dystrophic epidermolysis bullosa and uncovers new disease mechanisms. . 2015. PMID 26194911 · DOI · PMC4568953
- Costantino VV, Gil Lorenzo AF, Bocanegra V, Vallés PG. Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70. . 2021. PMID 34831368 · DOI · PMC8619557
- Puntmann VO, Nagel E, Beitzke D, Kammerlander A, Voges I, Doerr M, et al.. Losartan and prednisolone for post-COVID syndrome and cardiac inflammation: a randomized, double-blind, placebo-controlled trial. . 2026. PMID 42533000 · DOI · PMC13424660
- Sica DA, Gehr TW, Ghosh S. Clinical pharmacokinetics of losartan. Clin Pharmacokinet. 2005. PMID 16029066 · DOI
- Alderman M, Aiyer KJ. Uric acid: role in cardiovascular disease and effects of losartan. Curr Med Res Opin. 2004. PMID 15025846 · DOI
- Conlin PR, Spence JD, Williams B, Ribeiro AB, Saito I, Benedict C, et al.. Angiotensin II antagonists for hypertension: are there differences in efficacy?. Am J Hypertens. 2000. PMID 10821345 · DOI
- Warner KK, Visconti JA, Tschampel MM. Angiotensin II receptor blockers in patients with ACE inhibitor-induced angioedema. Ann Pharmacother. 2000. PMID 10772441 · DOI
- Matt P, Habashi J, Carrel T, Cameron DE, Van Eyk JE, Dietz HC. Recent advances in understanding Marfan syndrome: should we now treat surgical patients with losartan?. J Thorac Cardiovasc Surg. 2008. PMID 18242274 · DOI
- McIntyre M, Caffe SE, Michalak RA, Reid JL. Losartan, an orally active angiotensin (AT1) receptor antagonist: a review of its efficacy and safety in essential hypertension. Pharmacol Ther. 1997. PMID 9336021 · 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.