Evidence map›Paper›PMID 20126511›Full record

ArticleFuture medicinal chemistry2009

Future of anticathepsin K drugs: dual therapy for skeletal disease and atherosclerosis?

Izabela Podgorski

Open access · greenAbstract read
In one paragraph

Article in Future medicinal chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
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  7. Role of odanacatib in reducing bone loss due to endodontic disease: An overview.Journal of International Society of Preventive & Community Dentistry · 2016
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Structural basis of collagen fiber degradation by cathepsin K.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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

1 author at 1 institution in 1 country.

Izabela PodgorskiDepartment of Pharmacology, Wayne State University School of Medicine, 540 E. Canfield, Rm 6304, Detroit, MI 48201, USA. ipodgors@med.wayne.edu
Wayne State University · US

Funding

CATHEPSINS IN MALIGNANT PROGRESSION OF MCF 10R01CA056586 · NCI · WAYNE STATE UNIVERSITY · PI SLOANE, BONNIE F · 1992 to 2009
$3.3M
NCI NIH HHS R01 CA056586NCI NIH HHS R01 CA56586
6 · The paper itself

Abstract

backgroundUntil fairly recently, cathepsin K was recognized solely as a bone-resorbing enzyme expressed selectively in the osteoclast. Evidence of its requirement for normal bone remodeling has resulted in this protease receiving considerable attention from the pharmaceutical industry. In the last decade, intense research efforts were aimed at development of cathepsin K inhibitors for treatment of osteoporosis and other skeletal disorders associated with pathological bone loss. Emerging new evidence suggests that in addition to bone resorption, cathepsin K is involved in the turnover of extracellular matrix proteins in organs, such as the lung, thyroid and skin, and plays important roles in cardiovascular disease, inflammation and obesity. DISCUSSION: This review highlights the physiological and pathophysiological implications of this potent protease, with a focus on recent developments in the design and use of cathepsin K inhibitors to target skeletal pathologies. Therapeutic implications of anticathepsin K drugs in the context of common links between bone disease and atherosclerosis are also discussed.

conclusionThe association of cathepsin K with skeletal and cardiovascular disorders offers intriguing future applications for inhibitors of this potent protease.

Indexed as

AtherosclerosisBone DiseasesCathepsin KClinical Trials as TopicHumansOsteoporosisProtease InhibitorsCathepsin KProtease Inhibitors

Identifiers

PMID20126511
PMCPMC2780340
OpenAlexW2063359723

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.