Evidence map›Paper›PMID 23838168›Full record

ReviewThe international journal of biochemistry & cell biology2013

Calcineurin: a poorly understood regulator of muscle mass.

Matthew B Hudson, S Russ Price

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05029713 (Sarcopenic Obesity and Associated Risk Factors in Patients Undergone Liver Transplant), which is not on this map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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.

NCT05029713 completednot on this mapstarted 2021, after this paper: background citation

Sarcopenic Obesity and Associated Risk Factors in Patients Undergone Liver Transplant

TypeobservationalSponsorUniversity of BariRan2021 to 2023Enrolled400ConditionsSarcopenic ObesityArmsEvaluation of appendicular skeletal muscle mass (ASMM) by bioelectrical impedance analysis (BIA)
3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Undetected Neuromuscular Disease in Patients after Heart Transplantation.International journal of molecular sciences · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Ambient and supplemental magnetic fields promote myogenesisFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. Monitoring Kidney Dysfunction in Kugelberg-Welander Syndrome.The American journal of case reports · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Matthew B HudsonDepartment of Medicine, Renal Division, Emory University School of Medicine, Atlanta, GA 30322, United States. mbhudso@emory.edu
S Russ Price
Emory University · US

Funding

Nephrology Institutional Training Grant FLSA SupplementT32DK007656 · NIDDK · EMORY UNIVERSITY · PI SANDS, JEFF M, WALL, SUSAN MARIE · 1990 to 2020
$3.5M
Calcineurin signaling, PGC-1 alpha and protein-energy wasting in kidney diseaseR01DK095610 · NIDDK · EMORY UNIVERSITY · PI PRICE, S. RUSS · 2012 to 2015
$1.3M
Mechanisms of obesity-linked muscle atrophy and n-3 fatty acidsI01BX001456 · VA · VETERANS HEALTH ADMINISTRATION · PI PRICE, S. RUSS · 2013 to 2017
–
BLRD VA I01 BX001456NIDDK NIH HHS R01 DK095610NIDDK NIH HHS R01 DK-95610NIDDK NIH HHS T32 DK007656
6 · The paper itself

Abstract

This review will discuss the existing literature that has examined the role of calcineurin (CnA) in the regulation of skeletal muscle mass in conditions associated with hypertrophic growth or atrophy. Muscle mass is determined by the balance between protein synthesis and degradation which is controlled by a number of intracellular signaling pathways, most notably the insulin/IGF/phosphatidylinositol 3-kinase (PI3K)/Akt system. Despite being activated by IGF-1 and having well-described functions in the determination of muscle fiber phenotypes, calcineurin (CnA), a Ca(2+)-activated serine/threonine phosphatase, and its downstream signaling partners have garnered little attention as a regulator of muscle mass. Compared to other signaling pathways, the relatively few studies that have examined the role of CnA in the regulation of muscle size have produced discordant results. The reasons for these differences is not obvious but may be due to the selective nature of the genetic models studied, fluctuations in the endogenous level of CnA activity in various muscles, and the variable use of CnA inhibitors to inhibit CnA signaling. Despite the inconsistent nature of the outcomes, there is sufficient direct and indirect evidence to conclude that CnA plays a role in the regulation of skeletal muscle mass. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.

Indexed as

AnimalsCalcineurinHumansHypertrophyMice, TransgenicMuscle, SkeletalMuscular AtrophyPhosphorylationSignal TransductionCalcineurinAtrophycalcineurinCalcineurinCell signalingCnACnAαCnAββCsAcyclosporineForkhead box OFOXOHypertrophyIGF-1insulin-like growth factor-1isoform of the CnA catalytic subunitMCKMEF2MLCmuscle creatine kinasemyocyte enhancing factor 2myosin light chainNFATnuclear factor of activated T cellsphosphatidylinositol 3-kinasePI3KSkeletal muscleα isoform of the CnA catalytic subunit

Identifiers

PMID23838168
PMCPMC3947871
OpenAlexW1990026683

What OpenQuestion holds

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Registered trials

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.