Evidence map›Paper›PMID 28347910›Full record

ReviewBone2017

Acute lung injury complicating acute kidney injury: A model of endogenous αKlotho deficiency and distant organ dysfunction.

Connie C W Hsia, Priya Ravikumar, Jianfeng Ye

Abstract readReview
In one paragraph

Review in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Soft tissue calcifications in chronic kidney disease-beyond the vasculature.Pflugers Archiv : European journal of physiology · 2025
    Review
  4. Article
  5. Preeclampsia as a Study Model for Aging: The Klotho Gene Paradigm.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Constitutive transgenic α-Klotho overexpression enhances resilience to and recovery from murine acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

Connie C W HsiaDepartment of Internal Medicine, Pulmonary and Critical Care Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9034, United States of America. Electronic address: Connie.Hsia@utsouthwestern.edu.
Priya RavikumarDepartment of Internal Medicine, Pulmonary and Critical Care Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9034, United States of America; Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-9034, United States of America.
Jianfeng YeCharles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX 75390-9034, United States of America.
The University of Texas Southwestern Medical Center · US

Funding

Signals for Post-pneumonectomy Compensatory Lung GrowthR01HL040070 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HSIA, CONNIE C. W. · 1988 to 2014
$5.3M
Nanoparticle Drug Delivery in Post-Pneumonectomy Compensatory Lung GrowthU01HL111146 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HSIA, CONNIE C. W., NGUYEN, KYTAI TRUONG · 2012 to 2016
$3.2M
Structural Plasticity in Compensatory Lung Growth and RemodelingR01HL134373 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HSIA, CONNIE C. W. · 2017 to 2020
$2.8M
NHLBI NIH HHS R01 HL040070NHLBI NIH HHS R01 HL134373NHLBI NIH HHS U01 HL111146
6 · The paper itself

Abstract

The lung interfaces with atmospheric oxygen via a large surface area and is perfused by the entire venous return bearing waste products collected from the whole body. It is logical that the lung is endowed with generous anti-oxidative capacity derived both locally and from the circulation. The single-pass pleiotropic alpha-Klotho (αKlotho) protein was discovered when its genetic disruption led to premature multi-organ degeneration and early death. The extracellular domain of αKlotho is cleaved by secretases and released into circulation as endocrine soluble αKlotho protein, exerting wide-ranging cytoprotective effects including anti-oxidation on distant organs including the lung, which exhibits high sensitivity to circulating αKlotho insufficiency. Because circulating αKlotho is derived mainly from the kidney, acute kidney injury (AKI) leads to systemic αKlotho deficiency that in turn increases the risks of pulmonary complications, i.e., edema and inflammation, culminating in the acute respiratory distress syndrome. Exogenous αKlotho increases endogenous anti-oxidative capacity partly via activation of the Nrf2 pathway to protect lungs against injury caused by direct hyperoxia exposure or AKI. This article reviews the current knowledge of αKlotho antioxidation in the lung in the setting of AKI as a model of circulating αKlotho deficiency, an under-recognized condition that weakens innate cytoprotective defenses and contributes to the dysfunction in distant organs.

Indexed as

Acute Kidney InjuryAcute Lung InjuryAnimalsAntioxidantsHumansKidneyRenal Insufficiency, ChronicRespiratory Distress SyndromeAntioxidantsAcute respiratory distress syndromeAntioxidationCytoprotectionHyperoxiaNrf2 antioxidantsOxidative stress

Identifiers

PMID28347910
PMCPMC5621379
OpenAlexW2602915668

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.