Evidence map›Paper›PMID 23465499›Full record

ReviewSeminars in nephrology2013

Renal and extrarenal actions of Klotho.

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

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in nephrology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
9.0field-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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

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

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 at 1 institution in 1 country.

Ming Chang HuCharles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-8885, USA. ming.chang.hu@utsouthwestern.edu
Makoto Kuro-o
Orson W Moe
The University of Texas Southwestern Medical Center · US

Funding

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-DK-07938NIDDK NIH HHS R01 DK091392NIDDK NIH HHS R01-DK091392NIDDK NIH HHS R01 DK092461NIDDK NIH HHS R01-DK092461
6 · The paper itself

Abstract

Klotho is a single-pass transmembrane protein highly expressed in the kidney. Membrane Klotho protein acts as a co-receptor for fibroblast growth factor-23. Its extracellular domain is shed from the cell surface and functions as an endocrine substance that exerts multiple renal and extrarenal functions. An exhaustive review is beyond the scope and length of this article; thus, only effects with pertinence to mineral metabolism and renoprotection are highlighted here. Klotho participates in mineral homeostasis via interplay with other calciophosphoregulatory hormones (parathyroid hormone, fibroblast growth factor-23, and 1,25-[OH]2 vitamin D3) in kidney, bone, intestine, and parathyroid gland. Klotho also may be involved in acute and chronic kidney disease development and progression. Acute kidney injury is a temporary and reversible state of Klotho deficiency and chronic kidney disease is a sustained state of systemic Klotho deficiency. Klotho deficiency renders the kidney more susceptible to acute insults, delays kidney regeneration, and promotes renal fibrosis. In addition to direct renal effects, Klotho deficiency also triggers and aggravates deranged mineral metabolism, secondary hyperparathyroidism, vascular calcification, and cardiac hypertrophy and fibrosis. Although studies examining the therapeutic effect of Klotho replacement were performed in animal models, it is quite conceivable that supplementation of exogenous Klotho and/or up-regulation of endogenous Klotho production may be a viable therapeutic strategy for patients with acute or chronic kidney diseases.

Indexed as

Acute Kidney InjuryAnimalsCardiomegalyGlucuronidaseHumansHyperparathyroidism, SecondaryKidneyKlotho ProteinsMiceRatsRenal Insufficiency, ChronicVascular CalcificationGlucuronidaseKlotho Proteins

Identifiers

PMID23465499
PMCPMC3593734
OpenAlexW2016204066

What OpenQuestion holds

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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.