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 (768 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 52-amino acid peptide with multi-functions. It was originally isolated from pheochromocytoma and adrenal medulla but is widely distributed throughout the body including lung and kidney tissues. Besides controlling fluid-electrolyte homeostasis, adrenomedullin is a potent vasodilator and can inhibit pituitary ACTH secretion.
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: ADM (1-52); ADM(1-52); Adrenomedullin (1-52); PAMP(1-20)NH2; Proadrenomedullin (1-20); Proadrenomedullin N-Terminal 20 Peptide; Proadrenomedullin N Terminal 20 Peptide.
Where it fits in the MeSH classification
- Broader topics
- Peptide Hormones
Related concepts
Research landscape
PubMed indexes 3,310 records tagged with the MeSH heading “Adrenomedullin” (counts retrieved 2026-10-31). 398 of them (12.0%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 1,427 records.
Reviews account for 357 records (10.8%) and meta-analyses for 10. Randomized controlled trials number 66 (2.0%) 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 | 547 |
| 2000-2009 | 1,427 |
| 2010-2019 | 938 |
| 2020 onward | 398 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 357 | 10.8% |
| Meta-analyses | 10 | 0.3% |
| Randomized controlled trials | 66 | 2.0% |
Method: PubMed query "Adrenomedullin"[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 |
|---|---|---|---|---|
| Plasma adrenomedullin is associated with short-term mortality and vasopressor requirement in patients admitted with sepsis | 2014 | Research article Design not recorded in structured metadata | 110 | cc by PMID 24533868 · DOI · PMC4056312 |
| Adrenomedullin and tumour microenvironment | 2014 | Review article Design not recorded in structured metadata | 61 | cc by PMID 25475159 · DOI · PMC4272513 |
| Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells | 2021 | Research article Design not recorded in structured metadata | 59 | cc by PMID 33462236 · DOI · PMC7813857 |
| An RNA vaccine against adrenomedullin reduces angiogenesis and tumor burden in a syngeneic metastatic melanoma mouse model | 2025 | Research article Design not recorded in structured metadata | 7 | cc by PMID 40539045 · DOI · PMC12176902 |
Plasma adrenomedullin is associated with short-term mortality and vasopressor requirement in patients admitted with sepsis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionThe incidence of death among patients admitted for severe sepsis or septic shock is high.
- Closing excerpt
- 46; P ConclusionsIn patients admitted with sepsis, severe sepsis or septic shock plasma ADM is strongly associated with severity of disease, vasopressor requirement and 28-day mortality.
- 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 (176 words)
IntroductionThe incidence of death among patients admitted for severe sepsis or septic shock is high. Adrenomedullin (ADM) plays a central role in initiating the hyperdynamic response during the early stages of sepsis. Pilot studies indicate an association of plasma ADM with the severity of the disease. In the present study we utilized a novel sandwich immunoassay of bioactive plasma ADM in patients hospitalized with sepsis in order to assess the clinical utility.MethodsWe enrolled 101 consecutive patients admitted to the emergency department with suspected sepsis in this study. Sepsis was defined by fulfillment of at least two systemic inflammatory response syndrome (SIRS) criteria plus clinical suspicion of infection. Plasma samples for ADM measurement were obtained on admission and for the next four days. The 28-day mortality rate was recorded.ResultsADM at admission was associated with severity of disease (correlation with Acute Physiology and Chronic Health Evaluation II (APACHE II) score: r = 0.46; P ConclusionsIn patients admitted with sepsis, severe sepsis or septic shock plasma ADM is strongly associated with severity of disease, vasopressor requirement and 28-day mortality.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 24533868 · DOI · PMC4056312
Adrenomedullin and tumour microenvironment [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Adrenomedullin (AM) is a regulatory peptide whose involvement in tumour progression is becoming more relevant with recent studies.
- Closing excerpt
- In conclusion, AM is a great target for drug development and new drugs interfering with this system are being developed.
- 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)
Adrenomedullin (AM) is a regulatory peptide whose involvement in tumour progression is becoming more relevant with recent studies. AM is produced and secreted by the tumour cells but also by numerous stromal cells including macrophages, mast cells, endothelial cells, and vascular smooth muscle cells. Most cancer patients present high levels of circulating AM and in some cases these higher levels correlate with a worst prognosis. In some cases it has been shown that the high AM levels return to normal following surgical removal of the tumour, thus indicating the tumour as the source of this excessive production of AM. Expression of this peptide is a good investment for the tumour cell since AM acts as an autocrine/paracrine growth factor, prevents apoptosis-mediated cell death, increases tumour cell motility and metastasis, induces angiogenesis, and blocks immunosurveillance by inhibiting the immune system. In addition, AM expression gets rapidly activated by hypoxia through a HIF-1α mediated mechanism, thus characterizing AM as a major survival factor for tumour cells. Accordingly, a number of studies have shown that inhibition of this peptide or its receptors results in a significant reduction in tumour progression. In conclusion, AM is a great target for drug development and new drugs interfering with this system are being developed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25475159 · DOI · PMC4272513
Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Drug tolerant/resistant leukemic stem cell (LSC) subpopulations may explain frequent relapses in acute myeloid leukemia (AML), suggesting that these relapse-initiating cells (RICs) persistent after chemotherapy represent bona fide targets to prevent drug resistance and relapse.
- Closing excerpt
- In summary, our data highlight a critical role of ADM-CALCRL in post-chemotherapy persistence of these cells, and disclose a promising therapeutic target to prevent relapse in AML.
- 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 (142 words)
Drug tolerant/resistant leukemic stem cell (LSC) subpopulations may explain frequent relapses in acute myeloid leukemia (AML), suggesting that these relapse-initiating cells (RICs) persistent after chemotherapy represent bona fide targets to prevent drug resistance and relapse. We uncover that calcitonin receptor-like receptor (CALCRL) is expressed in RICs, and that the overexpression of CALCRL and/or of its ligand adrenomedullin (ADM), and not CGRP, correlates to adverse outcome in AML. CALCRL knockdown impairs leukemic growth, decreases LSC frequency, and sensitizes to cytarabine in patient-derived xenograft models. Mechanistically, the ADM-CALCRL axis drives cell cycle, DNA repair, and mitochondrial OxPHOS function of AML blasts dependent on E2F1 and BCL2. Finally, CALCRL depletion reduces LSC frequency of RICs post-chemotherapy in vivo. In summary, our data highlight a critical role of ADM-CALCRL in post-chemotherapy persistence of these cells, and disclose a promising therapeutic target to prevent relapse in AML.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33462236 · DOI · PMC7813857
An RNA vaccine against adrenomedullin reduces angiogenesis and tumor burden in a syngeneic metastatic melanoma mouse model [4]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionAdrenomedullin (AM) is an autocrine/paracrine growth factor as well as a crucial regulator of angiogenesis and immune response.
- Closing excerpt
- DiscussionIn summary, we have shown that an mRNA vaccine against the fusion KLH-AM peptide was able to break peripheral immunotolerance and induce a specific response against the angiogenic factor AM thus reducing tumor burden in the absence of disturbances to normal blood vessels.
- 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 (243 words)
IntroductionAdrenomedullin (AM) is an autocrine/paracrine growth factor as well as a crucial regulator of angiogenesis and immune response. AM is overexpressed by most solid tumors, which makes it a good target for anti-tumor therapy.MethodsIn this study, we designed and tested an mRNA vaccine directed against a fusion antigen composed by a small piece of keyhole limpet hemocyanin (KLH), as a hapten, and mouse AM. The in vitro-synthesized mRNA was encapsulated in lipid nanoparticles (LNPs) and injected in C57BL/6 mice. Empty LNPs were used as a negative control. After five immunizations, B16-F10 melanoma cells were injected through the tail vein to induce lung metastases. In addition, transgenic mice expressing green fluorescent protein in the blood vessels (SMAA-GFP) were also immunized with both LNP types to assess the potential side-effects of the vaccine on normal blood vessels.ResultsAntibody titers against AM and the number of CD8+ T cells were significantly higher in AM-immunized mice than in negative controls. Furthermore, the number and size of the lung metastases, as well as the number of blood vessels, were significantly reduced in the AM-immunized group. In addition, no significant differences were observed in the number and distribution of existing blood vessels after immunization of the SMAA-GFP animals.DiscussionIn summary, we have shown that an mRNA vaccine against the fusion KLH-AM peptide was able to break peripheral immunotolerance and induce a specific response against the angiogenic factor AM thus reducing tumor burden in the absence of disturbances to normal blood vessels.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40539045 · DOI · PMC12176902
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 Adrenomedullin in heart failure: pathophysiology and therapeutic application [5]
- Research article Therapeutic Targets for Heart Failure Identified Using Proteomics and Mendelian Randomization [6]
- Research article Adrenomedullin and Adrenomedullin-Targeted Therapy As Treatment Strategies Relevant for Sepsis [7]
- Research article Adrenomedullin and endothelial barrier function [8]
- Research article CGRP in the trigeminovascular system: a role for CGRP, adrenomedullin and amylin receptors? [9]
- Research article Pathophysiologic and therapeutic implications of adrenomedullin in cardiovascular disorders [10]
References
- Marino R, Struck J, Maisel AS, Magrini L, Bergmann A, Di Somma S. Plasma adrenomedullin is associated with short-term mortality and vasopressor requirement in patients admitted with sepsis. . 2014. PMID 24533868 · DOI · PMC4056312
- Larráyoz IM, Martínez-Herrero S, García-Sanmartín J, Ochoa-Callejero L, Martínez A. Adrenomedullin and tumour microenvironment. . 2014. PMID 25475159 · DOI · PMC4272513
- Larrue C, Guiraud N, Mouchel PL, Dubois M, Farge T, Gotanègre M, et al.. Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells. . 2021. PMID 33462236 · DOI · PMC7813857
- Tadic S, Ochoa-Callejero L, Narro-Íñiguez J, García-Sanmartín J, Martínez A. An RNA vaccine against adrenomedullin reduces angiogenesis and tumor burden in a syngeneic metastatic melanoma mouse model. . 2025. PMID 40539045 · DOI · PMC12176902
- Voors AA, Kremer D, Geven C, Ter Maaten JM, Struck J, Bergmann A, et al.. Adrenomedullin in heart failure: pathophysiology and therapeutic application. Eur J Heart Fail. 2019. PMID 30592365 · DOI · PMC6607488
- Henry A, Gordillo-Marañón M, Finan C, Schmidt AF, Ferreira JP, Karra R, et al.. Therapeutic Targets for Heart Failure Identified Using Proteomics and Mendelian Randomization. Circulation. 2022. PMID 35300523 · DOI · PMC9010023
- Geven C, Kox M, Pickkers P. Adrenomedullin and Adrenomedullin-Targeted Therapy As Treatment Strategies Relevant for Sepsis. Front Immunol. 2018. PMID 29520277 · DOI · PMC5827550
- Temmesfeld-Wollbrück B, Hocke AC, Suttorp N, Hippenstiel S. Adrenomedullin and endothelial barrier function. Thromb Haemost. 2007. PMID 18000597 · DOI
- Walker CS, Hay DL. CGRP in the trigeminovascular system: a role for CGRP, adrenomedullin and amylin receptors?. Br J Pharmacol. 2013. PMID 23425327 · DOI · PMC3838677
- Ishimitsu T, Ono H, Minami J, Matsuoka H. Pathophysiologic and therapeutic implications of adrenomedullin in cardiovascular disorders. Pharmacol Ther. 2006. PMID 16616959 · 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.