Evidence map›Paper›PMID 26669699›Full record

ArticleCell metabolism2016

PTH/PTHrP Receptor Mediates Cachexia in Models of Kidney Failure and Cancer.

Serkan Kir, Hirotaka Komaba, Ana P Garcia, Konstantinos P Economopoulos, Wei Liu, Beate Lanske, Richard A Hodin, Bruce M Spiegelman

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 2 pooled it
13.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

189 citing papers in PubMed, 2 syntheses or guidelines pooled it, 305 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Parathyroid hormone enhances appetite and fails to reduce adiposity in ob/ob mice.Pflugers Archiv : European journal of physiology · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

129 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Serkan KirDepartment of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Hirotaka KomabaDepartment of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Ana P GarciaDepartment of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Konstantinos P EconomopoulosDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Wei LiuDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Beate LanskeDepartment of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Richard A HodinDepartment of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Bruce M SpiegelmanDepartment of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. Electronic address: bruce_spiegelman@dfci.harvard.edu.
Harvard University · US

Funding

CONTROL OF ADIPOCYTE GENE EXPRESSION AND PHYSIOLOGYR37DK031405 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1996 to 2013
$8.2M
CONTROL OF LIPOGENIC ENZYME SYNTHESIS IN ADIPOCYTESR01DK031405 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI SPIEGELMAN, BRUCE M. · 1986 to 2018
$2.9M
The Regulation of the Parathyroid GlandR01DK097105 · NIDDK · HARVARD MEDICAL SCHOOL · PI MANNSTADT, BEATE · 2012 to 2015
$2.2M
Roles of tumor-derived PTHrP in skeletal muscle atrophy and cancer cachexiaK99CA197410 · NCI · DANA-FARBER CANCER INST · PI KIR, SERKAN · 2016 to 2017
$245k
NCI NIH HHS K99 CA197410NIDDK NIH HHS DK097105NIDDK NIH HHS DK31405NIDDK NIH HHS R01 DK031405NIDDK NIH HHS R01 DK097105NIDDK NIH HHS R37 DK031405
6 · The paper itself

Abstract

Cachexia is a wasting syndrome associated with elevated basal energy expenditure and loss of adipose and muscle tissues. It accompanies many chronic diseases including renal failure and cancer and is an important risk factor for mortality. Our recent work demonstrated that tumor-derived PTHrP drives adipose tissue browning and cachexia. Here, we show that PTH is involved in stimulating a thermogenic gene program in 5/6 nephrectomized mice that suffer from cachexia. Fat-specific knockout of PTHR blocked adipose browning and wasting. Surprisingly, loss of PTHR in fat tissue also preserved muscle mass and improved muscle strength. Similarly, PTHR knockout mice were resistant to cachexia driven by tumors. Our results demonstrate that PTHrP and PTH mediate wasting through a common mechanism involving PTHR, and there exists an unexpected crosstalk mechanism between wasting of fat tissue and skeletal muscle. Targeting the PTH/PTHrP pathway may have therapeutic uses in humans with cachexia.

Indexed as

Adipose TissueAnimalsAtrophyCachexiaCarcinoma, Lewis LungDisease Models, AnimalGene Expression RegulationHyperparathyroidismIon ChannelsMaleMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsMuscle, SkeletalNephrectomyParathyroid HormoneIon ChannelsMitochondrial ProteinsParathyroid HormoneParathyroid Hormone-Related ProteinReceptor, Parathyroid Hormone, Type 1Uncoupling Protein 1adipose tissue browningcachexiacancerchronic kidney diseaseparathyroid hormone (PTH)PTHrPskeletal muscle atrophy

Identifiers

PMID26669699
PMCPMC4749423
OpenAlexW2190022467

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.