Evidence map›Paper›PMID 23761674›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Regulation of urinary ACE2 in diabetic mice.

Jan Wysocki, Laura Garcia-Halpin, Minghao Ye, Christoph Maier, Kurt Sowers, Kevin D Burns, Daniel Batlle

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
–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

44 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Review
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  13. Review
  14. An update on ACE2 amplification and its therapeutic potential.Acta physiologica (Oxford, England) · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Existence of SARS-CoV-2 Entry Molecules in the Oral Cavity.International journal of molecular sciences · 2020
    Article
  20. SARS-CoV-2 perturbs the renin-angiotensin system and energy metabolism.American journal of physiology. Endocrinology and metabolism · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Jan WysockiDiv. of Nephrology and Hypertension, Dept. of Medicine, The Feinberg School of Medicine, Northwestern Univ., 320 E. Superior, Chicago, IL 60611. d-batlle@northwestern.edu.
Laura Garcia-Halpin
Minghao Ye
Christoph Maier
Kurt Sowers
Kevin D Burns
Daniel Batlle

Funding

Strategies for ACE2 Amplification to Treat Diabetic Kidney DiseaseR01DK080089 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BATLLE, DANIEL · 2009 to 2012
$1.3M
ACE and ACE2 in Glomerular Angiotensin Peptides MetabolismF32DK079546 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI WYSOCKI, JAN ANDRZEJ · 2008 to 2010
$118k
NIDDK NIH HHS 1R-01-DK-080089-01A2NIDDK NIH HHS F32-DK-079546NIDDK NIH HHS R01 DK080089
6 · The paper itself

Abstract

Angiotensin-converting enzyme-2 (ACE2) enhances the degradation of ANG II and its expression is altered in diabetic kidneys, but the regulation of this enzyme in the urine is unknown. Urinary ACE2 was studied in the db/db model of type 2 diabetes and stretozotocin (STZ)-induced type 1 diabetes during several physiological and pharmacological interventions. ACE2 activity in db/db mice was increased in the serum and to a much greater extent in the urine compared with db/m controls. Neither a specific ANG II blocker, telmisartan, nor an ACE inhibitor, captopril, altered the levels of urinary ACE2 in db/db or db/m control mice. High-salt diet (8%) increased whereas low-salt diet (0.1%) decreased urinary ACE2 activity in the urine of db/db mice. In STZ mice, urinary ACE2 was also increased, and insulin decreased it partly but significantly after several weeks of administration. The increase in urinary ACE2 activity in db/db mice reflected an increase in enzymatically active protein with two bands identified of molecular size at 110 and 75 kDa and was associated with an increase in kidney cortex ACE2 protein at 110 kDa but not at 75 kDa. ACE2 activity was increased in isolated tubular preparations but not in glomeruli from db/db mice. Administration of soluble recombinant ACE2 to db/m and db/db mice resulted in a marked increase in serum ACE2 activity, but no gain in ACE2 activity was detectable in the urine, further demonstrating that urinary ACE2 is of kidney origin. Increased urinary ACE2 was associated with more efficient degradation of exogenous ANG II (10(-9) M) in urine from db/db compared with that from db/m mice. Urinary ACE2 could be a potential biomarker of increased metabolism of ANG II in diabetic kidney disease.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IIAnimalsBiomarkersBlotting, WesternDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Diabetic NephropathiesFemaleMaleMiceMice, Inbred C57BLPeptidyl-Dipeptidase AAce2 protein, mouseAngiotensin-Converting Enzyme 2Angiotensin IIBiomarkersPeptidyl-Dipeptidase Aangiotensin-converting enzyme 2biomarkerdiabetesnephropathyurinary

Identifiers

PMID23761674
PMCPMC3891267

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.