Argatroban Attenuates Diabetic Cardiomyopathy in Rats by Reducing Fibrosis, Inflammation, Apoptosis, and Protease-Activated Receptor Expression

Argatroban Attenuates Diabetic Cardiomyopathy in Rats by Reducing Fibrosis, Inflammation,... Purpose Chronic diabetes is associated with cardiovascular functional disturbances as evidenced from impaired cardiac dysfunctions. Diabetic cardiomyopathy (DCM) is one of the functional parameters and increased fibrosis. There was a sig- serious cardiovascular complications associated with diabetes. nificant increase in PAR expression after 20 weeks of diabetes Despite significant efforts in understanding the pathophysiol- induction. Four weeks argatroban treatment ameliorated met- ogy of DCM, management of DCM is not adequate due to its abolic alterations (reduced plasma glucose and cholesterol), complex pathophysiology. Recently, involvement of protease- ventricular dysfunctions (improved systolic and diastolic activated receptors (PARs) has been postulated in cardiovas- functions), cardiac fibrosis (reduced percentage area of colla- cular diseases. These receptors are activated by thrombin, gen in picro-sirius red staining), and apoptosis (reduced trypsin, or other serine proteases. Expression of PAR has been TUNEL positive nuclei). Reduced expression of PAR1 and shown to be increased in cardiac diseases such as myocardial PAR4 in the argatroban-treated group indicates a response infarction, viral myocarditis, and pulmonary arterial hyperten- towards inhibition of thrombin. In addition, AKT (Ser-473), sion. However, the role of PAR in DCM has not been eluci- GSK-3β (Ser-9), p-65 NFĸB phosphorylation, TGF-β,COX- dated yet. Therefore, in the present http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cardiovascular Drugs and Therapy Springer Journals

Argatroban Attenuates Diabetic Cardiomyopathy in Rats by Reducing Fibrosis, Inflammation, Apoptosis, and Protease-Activated Receptor Expression

Loading next page...
 
/lp/springer_journal/argatroban-attenuates-diabetic-cardiomyopathy-in-rats-by-reducing-JfMMavr84O
Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Medicine & Public Health; Cardiology
ISSN
0920-3206
eISSN
1573-7241
D.O.I.
10.1007/s10557-017-6732-3
Publisher site
See Article on Publisher Site

Abstract

Purpose Chronic diabetes is associated with cardiovascular functional disturbances as evidenced from impaired cardiac dysfunctions. Diabetic cardiomyopathy (DCM) is one of the functional parameters and increased fibrosis. There was a sig- serious cardiovascular complications associated with diabetes. nificant increase in PAR expression after 20 weeks of diabetes Despite significant efforts in understanding the pathophysiol- induction. Four weeks argatroban treatment ameliorated met- ogy of DCM, management of DCM is not adequate due to its abolic alterations (reduced plasma glucose and cholesterol), complex pathophysiology. Recently, involvement of protease- ventricular dysfunctions (improved systolic and diastolic activated receptors (PARs) has been postulated in cardiovas- functions), cardiac fibrosis (reduced percentage area of colla- cular diseases. These receptors are activated by thrombin, gen in picro-sirius red staining), and apoptosis (reduced trypsin, or other serine proteases. Expression of PAR has been TUNEL positive nuclei). Reduced expression of PAR1 and shown to be increased in cardiac diseases such as myocardial PAR4 in the argatroban-treated group indicates a response infarction, viral myocarditis, and pulmonary arterial hyperten- towards inhibition of thrombin. In addition, AKT (Ser-473), sion. However, the role of PAR in DCM has not been eluci- GSK-3β (Ser-9), p-65 NFĸB phosphorylation, TGF-β,COX- dated yet. Therefore, in the present

Journal

Cardiovascular Drugs and TherapySpringer Journals

Published: Jul 10, 2017

References

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create lists to
organize your research

Export lists, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off