Evidence map›Paper›PMID 24867676›Full record

ReviewCurrent opinion in nephrology and hypertension2014

αKlotho and vascular calcification: an evolving paradigm.

Ming Chang Hu, Makoto Kuro-o, Orson W Moe

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. A Land of Controversy: Fibroblast Growth Factor-23 and Uremic Cardiac Hypertrophy.Journal of the American Society of Nephrology : JASN · 2020
    Review
  7. Article
  8. The tripartite interaction of phosphate, autophagy, and αKlotho in health maintenance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  9. Salusin-β Promotes Vascular CalcificationAntioxidants & redox signaling · 2019
    Article
  10. Article
  11. Article
  12. Growth Hormone (GH) and Cardiovascular System.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. αKlotho and Chronic Kidney Disease.Vitamins and hormones · 2016
    Review
  16. Alpha Klotho and phosphate homeostasis.Journal of endocrinological investigation · 2014
    Review
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

3 authors.

Ming Chang HuaDepartment of Internal Medicine bThe Charles and Jane Pak Center of Mineral Metabolism and Clinical Research cDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA dCenter for Molecular Medicine, Jichi Medical University Tochigi, Japan eDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Makoto Kuro-o
Orson W Moe

Funding

UT Southwestern O'Brien Kidney Research Core CenterP30DK079328 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 2007 to 2021
$16.9M
Klotho: Therapeutic Agent for Ischemia Reperfusion Induced Acute Kidney InjuryR01DK092461 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HU, MING-CHANG · 2011 to 2021
$3.7M
Klotho and Phosphate in Chronic Kidney Disease: Pathogenesis and TherapeuticsR01DK091392 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI HU, MING-CHANG, MOE, ORSON W · 2011 to 2021
$3.2M
ENDOCRINE REGULATION OF MUSCLE GROWTH &DIFFERENTIATIONF32DK007938 · NIDDK · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI MCCUSKER, ROBERT H. · 1986 to 1987
–
NIDDK NIH HHS P30 DK079328NIDDK NIH HHS (P30-DK-07938NIDDK NIH HHS R01 DK091392NIDDK NIH HHS R01-DK091392NIDDK NIH HHS R01 DK092461NIDDK NIH HHS R01-DK092461
6 · The paper itself

Abstract

purpose of reviewCardiovascular disease remains the single most serious contributor to mortality in chronic kidney disease (CKD). Although conventional risk factors are prevalent in CKD, both cardiomyopathy and vasculopathy can be caused by pathophysiologic mechanisms specific to the uremic state. CKD is a state of systemic αKlotho deficiency. Although the molecular mechanism of action of αKlotho is not well understood, the downstream targets and biologic functions of αKlotho are astonishingly pleiotropic. An emerging body of literature links αKlotho to uremic vasculopathy. RECENT

findingsThe expression of αKlotho in the vasculature is controversial because of conflicting data. Regardless of whether αKlotho acts as a circulating or resident protein, there are good data associating changes in αKlotho levels with vascular pathology including vascular calcification and in-vitro data of the direct action of αKlotho on both the endothelium and vascular smooth muscle cells in terms of cytoprotection and prevention of mineralization. SUMMARY: It is critical to understand the pathogenic role of αKlotho on the integral endothelium-vascular smooth muscle network rather than each cell type in isolation in uremic vasculopathy, as αKlotho can serve as a potential prognostic biomarker and a biological therapeutic agent.

Indexed as

AnimalsEndotheliumGlucuronidaseHumansKlotho ProteinsMuscle, Smooth, VascularRenal Insufficiency, ChronicUremiaVascular CalcificationVascular StiffnessGlucuronidaseKlotho Proteins

Identifiers

PMID24867676
PMCPMC4141856

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.