Evidence map›Paper›PMID 26774586›Full record

ArticlePeptides2016

Cardiorenal fibrosis and dysfunction in aging: Imbalance in mediators and regulators of collagen.

S Jeson Sangaralingham, Bing H Wang, Li Huang, Sirinart Kumfu, Tomoko Ichiki, Henry Krum, John C Burnett

Abstract read
In one paragraph

Article in Peptides, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Loss of Natriuretic Peptide Receptor C Enhances Sinoatrial Node Dysfunction in Aging and Frail Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
    Article
  8. Review
  9. The Signaling of Cellular Senescence in Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2019
    Review
  10. Review
  11. Article
  12. Chronic treatment with the mitochondrial peptide humanin prevents age-related myocardial fibrosis in mice.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  13. Review
  14. Article
  15. Renal Aging: Causes and Consequences.Journal of the American Society of Nephrology : JASN · 2017
    Review
  16. Drugs and Targets in Fibrosis.Frontiers in pharmacology · 2017
    Review
  17. Innovative Therapeutics: Designer Natriuretic Peptides.JACC. Basic to translational science · 2016
    Article
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

S Jeson SangaralinghamCardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA. Electronic address: sangaralingham.jeson@mayo.edu.
Bing H WangCentre of Cardiovascular Research and Education in Therapeutics, School of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Li HuangCentre of Cardiovascular Research and Education in Therapeutics, School of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Sirinart KumfuCentre of Cardiovascular Research and Education in Therapeutics, School of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Tomoko IchikiCardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA.
Henry KrumCentre of Cardiovascular Research and Education in Therapeutics, School of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
John C BurnettCardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA.
Monash University · AUMayo Clinic in Florida · US

Funding

Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
Recruitment and Phenotyping CoreP01HL076611 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C · 2005 to 2015
$19.6M
Cardiovascular Peptides and Myocardial InfarctionR01HL083231 · NHLBI · MAYO CLINIC ROCHESTER · PI BURNETT, JOHN C, CHEN, HORNG H · 2006 to 2016
$4.6M
NCATS NIH HHS UL1 TR000135NHLBI NIH HHS P01 HL076611NHLBI NIH HHS P01-HL076611NHLBI NIH HHS R01 HL083231NHLBI NIH HHS R01-HL083231
6 · The paper itself

Abstract

Cardiorenal fibrosis is a biological process that increases with age and contributes to dysfunction of the heart and kidney. While numerous circulating and tissue hormones, cytokines and enzymes have been identified in the development of cardiorenal fibrosis, several reports have suggested that the anti-fibrotic natriuretic peptide system (NPS), pro-fibrotic renin-angiotensin-aldosterone system (RAAS), transforming growth factor-beta 1 (TGF-β1), matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) are fundamental regulators and mediators of this process. However, the simultaneous assessment of these components in the development of age-mediated cardiorenal fibrotic remodeling is not completely understood. Thus, we assessed cardiorenal structure and function, the circulating NPS and RAAS and the cardiorenal tissue gene expression of collagen (Col) I, Col III, TGF-β1, MMP-9 and TIMP-1 in 2 and 20 month old Fischer rats. Our studies determined that aging was characterized by an increase in cardiorenal fibrosis that was accompanied with cardiorenal dysfunction. These alterations were associated with lower circulating atrial and C-type natriuretic peptides and higher angiotensin II and aldosterone levels in the aged rats. Moreover, we observed a decrease in Col I and III and an increase in TIMP- mRNA expressions in the aged heart and kidney, while TGF-β1 expression increased and MMP-9 decreased only in the aged kidney. We conclude that the age-mediated alterations in these fibrotic regulator and mediator profiles favors collagen accumulation due to an imbalance between the NPS and RAAS as well as a decline in the degradative pathway, thus suggesting a therapeutic opportunity to target these components.

Indexed as

AgingAnimalsCollagenEndomyocardial FibrosisFibrosisGene ExpressionKidneyMaleMatrix Metalloproteinase 9MyocardiumNatriuretic PeptidesRats, Inbred F344Tissue Inhibitor of Metalloproteinase-1Transforming Growth Factor beta1CollagenMatrix Metalloproteinase 9Mmp9 protein, ratNatriuretic PeptidesTIMP1 protein, ratTissue Inhibitor of Metalloproteinase-1Transforming Growth Factor beta1CardiorenalFibrosisGene expressionNatriuretic peptidesRenin–angiotensin–aldosterone system

Identifiers

PMID26774586
PMCPMC4754975
OpenAlexW2234286907

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.