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 (655 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 ubiquitously expressed, secreted protein with bone resorption and renal calcium reabsorption activities that are similar to parathyroid hormone. It does not circulate in appreciable amounts in normal subjects, but rather exerts its biological actions locally. Overexpression of parathyroid hormone-related protein by tumor cells results in humoral calcemia of malignancy.
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: Hormone-Related Protein, Parathyroid; Parathyroid Hormone Related Protein; PTH-Related Peptide; PTH Related Peptide; Hypercalcemic Hormone of Malignancy; PTH Like Tumor Factor; PTH-Like Protein; PTH Like Protein.
Where it fits in the MeSH classification
- Broader topics
- Peptide Hormones; Intercellular Signaling Peptides and Proteins
- See also
- Parathyroid Hormone; Receptors, Parathyroid Hormone
Related concepts
Research landscape
PubMed indexes 3,616 records tagged with the MeSH heading “Parathyroid Hormone-Related Protein” (counts retrieved 2026-10-31). 340 of them (9.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,381 records.
Reviews account for 569 records (15.7%) and meta-analyses for 14. Randomized controlled trials number 39 (1.1%) 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 | 1,381 |
| 2000-2009 | 1,134 |
| 2010-2019 | 761 |
| 2020 onward | 340 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 569 | 15.7% |
| Meta-analyses | 14 | 0.4% |
| Randomized controlled trials | 39 | 1.1% |
Method: PubMed query "Parathyroid Hormone-Related Protein"[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 |
|---|---|---|---|---|
| ACTIVExtend: 24 Months of Alendronate After 18 Months of Abaloparatide or Placebo for Postmenopausal Osteoporosis | 2018 | Randomized controlled trial Design not recorded in structured metadata | 154 | cc by PMID 29800372 · DOI · PMC6097601 |
| The Wnt/beta-catenin pathway interacts differentially with PTHrP signaling to control chondrocyte hypertrophy and final maturation | 2009 | Research article Design not recorded in structured metadata | 68 | cc0 PMID 19557172 · DOI · PMC2698152 |
| A FoxA2+ long-term stem cell population is necessary for growth plate cartilage regeneration after injury | 2022 | Research article Design not recorded in structured metadata | 52 | cc by PMID 35523895 · DOI · PMC9076650 |
| Parathyroid hormone-related protein is a therapeutic target in idiopathic pulmonary fibrosis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 41724741 · DOI · PMC12926227 |
ACTIVExtend: 24 Months of Alendronate After 18 Months of Abaloparatide or Placebo for Postmenopausal Osteoporosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- PurposeIn women with postmenopausal osteoporosis, we investigated the effects of 24 months of treatment with alendronate (ALN) following 18 months of treatment with abaloparatide (ABL) or placebo (PBO).
- Closing excerpt
- Sequential ABL followed by ALN appears to be an effective treatment option for postmenopausal women at risk for osteoporosis-related fractures.
- 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 (181 words)
PurposeIn women with postmenopausal osteoporosis, we investigated the effects of 24 months of treatment with alendronate (ALN) following 18 months of treatment with abaloparatide (ABL) or placebo (PBO).MethodsWomen who completed ABL or PBO treatment in ACTIVE were eligible to receive up to 24 months of ALN. We evaluated the incidence of vertebral and nonvertebral fractures and changes in bone mineral density (BMD) during the entire 43-month period from ACTIVE baseline to the end of ACTIVExtend and for the 24-month extension only.ResultsFive hundred fifty-eight women from ACTIVE's ABL group and 581 from its PBO group (92% of ABL and PBO completers) were enrolled. During the full 43-month treatment period, 0.9% of evaluable women in the ABL/ALN group experienced a new radiographic vertebral fracture vs 5.6% of women in the PBO/ALN group, an 84% relative risk reduction (RRR, P ConclusionsEighteen months of ABL followed by 24 months of ALN reduced the risk of vertebral, nonvertebral, clinical, and major osteoporotic fractures and increased BMD. Sequential ABL followed by ALN appears to be an effective treatment option for postmenopausal women at risk for osteoporosis-related fractures.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29800372 · DOI · PMC6097601
The Wnt/beta-catenin pathway interacts differentially with PTHrP signaling to control chondrocyte hypertrophy and final maturation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Sequential proliferation, hypertrophy and maturation of chondrocytes are required for proper endochondral bone development and tightly regulated by cell signaling.
- Closing excerpt
- Furthermore, Wnt/beta-catenin signaling also controls final maturation of hypertrophic chondrocytes, but such regulation is PTHrP signaling-independent.
- 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 (126 words)
Sequential proliferation, hypertrophy and maturation of chondrocytes are required for proper endochondral bone development and tightly regulated by cell signaling. The canonical Wnt signaling pathway acts through beta-catenin to promote chondrocyte hypertrophy whereas PTHrP signaling inhibits it by holding chondrocytes in proliferating states. Here we show by genetic approaches that chondrocyte hypertrophy and final maturation are two distinct developmental processes that are differentially regulated by Wnt/beta-catenin and PTHrP signaling. Wnt/beta-catenin signaling regulates initiation of chondrocyte hypertrophy by inhibiting PTHrP signaling activity, but it does not regulate PTHrP expression. In addition, Wnt/beta-catenin signaling regulates chondrocyte hypertrophy in a non-cell autonomous manner and Gdf5/Bmp signaling may be one of the downstream pathways. Furthermore, Wnt/beta-catenin signaling also controls final maturation of hypertrophic chondrocytes, but such regulation is PTHrP signaling-independent.
Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 19557172 · DOI · PMC2698152
A FoxA2+ long-term stem cell population is necessary for growth plate cartilage regeneration after injury [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Longitudinal bone growth, achieved through endochondral ossification, is accomplished by a cartilaginous structure, the physis or growth plate, comprised of morphologically distinct zones related to chondrocyte function: resting, proliferating and hypertrophic zones.
- Closing excerpt
- When the growth plate is injured, FoxA2+ cells expand in response to trauma, and produce physeal cartilage for growth plate tissue regeneration.
- 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 (133 words)
Longitudinal bone growth, achieved through endochondral ossification, is accomplished by a cartilaginous structure, the physis or growth plate, comprised of morphologically distinct zones related to chondrocyte function: resting, proliferating and hypertrophic zones. The resting zone is a stem cell-rich region that gives rise to the growth plate, and exhibits regenerative capabilities in response to injury. We discovered a FoxA2+group of long-term skeletal stem cells, situated at the top of resting zone, adjacent the secondary ossification center, distinct from the previously characterized PTHrP+ stem cells. Compared to PTHrP+ cells, FoxA2+ cells exhibit higher clonogenicity and longevity. FoxA2+ cells exhibit dual osteo-chondro-progenitor activity during early postnatal development (P0-P28) and chondrogenic potential beyond P28. When the growth plate is injured, FoxA2+ cells expand in response to trauma, and produce physeal cartilage for growth plate tissue regeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35523895 · DOI · PMC9076650
Parathyroid hormone-related protein is a therapeutic target in idiopathic pulmonary fibrosis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The crosstalk between immune or alveolar epithelial cells and fibroblasts mediated by paracrine signaling molecules is associated with the pathogenesis of idiopathic pulmonary fibrosis (IPF).
- Closing excerpt
- In conclusion, our results suggest that PTHrP1-34 derived from bronchial epithelial cells is involved in the pathogenesis of IPF and is a promising target for alleviating disease progression.
- 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 (215 words)
The crosstalk between immune or alveolar epithelial cells and fibroblasts mediated by paracrine signaling molecules is associated with the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, studies investigating the active involvement of soluble mediators derived from bronchial epithelial cells in fibroblast activation and the development of pulmonary fibrosis are limited. Reanalysis of bulk and single-cell RNA-sequencing data from human bronchus and IPF lung tissue revealed marked upregulation of parathyroid hormone-like hormone (PTHLH) in IPF lung tissue compared with normal tissue, with expression predominantly localized to bronchial epithelial cells. parathyroid hormone-related protein (PTHrP) translated from PTHLH was significantly increased in the bronchial epithelium of IPF patients and bleomycin-induced pulmonary fibrosis mice. Furthermore, the paracrine peptide PTHrP1-34, generated through post-translational processing of PTHrP, was elevated in lung homogenates and bronchoalveolar lavage fluid obtained from fibrotic lungs. Cell- and animal-based experiments showed that PTHrP1-34 activated fibroblasts and extracellular matrix production, resulting in the progression of pulmonary fibrosis. In a preclinical evaluation using a bleomycin-induced pulmonary fibrosis mouse model, attenuating effects against pulmonary fibrosis were observed using neutralizing antibodies, peptides, and gene silencing strategies targeting the PTHrP1-34/parathyroid hormone 1 receptor axis. In conclusion, our results suggest that PTHrP1-34 derived from bronchial epithelial cells is involved in the pathogenesis of IPF and is a promising target for alleviating disease progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41724741 · DOI · PMC12926227
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 PTHrP and skeletal development [5]
- Research article PTH and PTHrP signaling in osteoblasts [6]
- Research article Parathyroid hormone and parathyroid hormone-related peptide, and their receptors [7]
- Research article Parathyroid hormone-related protein: an update [8]
- Research article Twenty-five years of PTHrP progress: from cancer hormone to multifunctional cytokine [9]
- Research article Parathyroid Hormone-Related Protein, Its Regulation of Cartilage and Bone Development, and Role in Treating Bone Diseases [10]
References
- Bone HG, Cosman F, Miller PD, Williams GC, Hattersley G, Hu MY, et al.. ACTIVExtend: 24 Months of Alendronate After 18 Months of Abaloparatide or Placebo for Postmenopausal Osteoporosis. . 2018. PMID 29800372 · DOI · PMC6097601
- Guo X, Mak KK, Taketo MM, Yang Y. The Wnt/beta-catenin pathway interacts differentially with PTHrP signaling to control chondrocyte hypertrophy and final maturation. . 2009. PMID 19557172 · DOI · PMC2698152
- Muruganandan S, Pierce R, Teguh DA, Perez RF, Bell N, Nguyen B, et al.. A FoxA2+ long-term stem cell population is necessary for growth plate cartilage regeneration after injury. . 2022. PMID 35523895 · DOI · PMC9076650
- Fang XQ, Lim S, Lee YM, Lim CH, Kim HB, Joo JH, et al.. Parathyroid hormone-related protein is a therapeutic target in idiopathic pulmonary fibrosis. . 2026. PMID 41724741 · DOI · PMC12926227
- Kronenberg HM. PTHrP and skeletal development. Ann N Y Acad Sci. 2006. PMID 16831900 · DOI
- Datta NS, Abou-Samra AB. PTH and PTHrP signaling in osteoblasts. Cell Signal. 2009. PMID 19249350 · DOI · PMC2723940
- Gensure RC, Gardella TJ, Jüppner H. Parathyroid hormone and parathyroid hormone-related peptide, and their receptors. Biochem Biophys Res Commun. 2005. PMID 15694400 · DOI
- Wysolmerski JJ. Parathyroid hormone-related protein: an update. J Clin Endocrinol Metab. 2012. PMID 22745236 · DOI · PMC3431578
- McCauley LK, Martin TJ. Twenty-five years of PTHrP progress: from cancer hormone to multifunctional cytokine. J Bone Miner Res. 2012. PMID 22549910 · DOI · PMC4871126
- Martin TJ. Parathyroid Hormone-Related Protein, Its Regulation of Cartilage and Bone Development, and Role in Treating Bone Diseases. Physiol Rev. 2016. PMID 27142453 · 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.