PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Combined Inhibition of the Renin-Angiotensin System and Neprilysin Positively Influences Complex Mitochondrial Adaptations in Progressive Experimental Heart Failure.

Abstract Inhibitors of the renin angiotensin system and neprilysin (RAS-/NEP-inhibitors) proved to be extraordinarily beneficial in systolic heart failure. Furthermore, compelling evidence exists that impaired mitochondrial pathways are causatively involved in progressive left ventricular (LV) dysfunction. Consequently, we aimed to assess whether RAS-/NEP-inhibition can attenuate mitochondrial adaptations in experimental heart failure (HF).
PMID
Related Publications

Combined neprilysin and renin-angiotensin system inhibition in heart failure with reduced ejection fraction: a meta-analysis.

Interatrial differences of basal molecular set-up and changes in tachycardia-induced heart failure-a proteomic profiling study.

SP 04-1 THE ROLE OF NATRIURETIC PEPTIDES IN THE PATHOGENESIS OF CARDIOVASCULAR DISEASES.

Proteomic profiling implies mitochondrial dysfunction in tachycardia-induced heart failure.

Antihypertrophic effects of combined inhibition of the renin-angiotensin system (RAS) and neutral endopeptidase (NEP) in progressive, tachycardia-induced experimental heart failure.

Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28076404
OWN - NLM
STAT- In-Data-Review
DA  - 20170111
LR  - 20170201
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 1
DP  - 2017
TI  - Combined Inhibition of the Renin-Angiotensin System and Neprilysin Positively
      Influences Complex Mitochondrial Adaptations in Progressive Experimental Heart
      Failure.
PG  - e0169743
LID - 10.1371/journal.pone.0169743 [doi]
AB  - BACKGROUND: Inhibitors of the renin angiotensin system and neprilysin
      (RAS-/NEP-inhibitors) proved to be extraordinarily beneficial in systolic heart
      failure. Furthermore, compelling evidence exists that impaired mitochondrial
      pathways are causatively involved in progressive left ventricular (LV)
      dysfunction. Consequently, we aimed to assess whether RAS-/NEP-inhibition can
      attenuate mitochondrial adaptations in experimental heart failure (HF). METHODS
      AND RESULTS: By progressive right ventricular pacing, distinct HF stages were
      induced in 15 rabbits, and 6 animals served as controls (CTRL). Six animals with 
      manifest HF (CHF) were treated with the RAS-/NEP-inhibitor omapatrilat.
      Echocardiographic studies and invasive blood pressure measurements were
      undertaken during HF progression. Mitochondria were isolated from LV tissue,
      respectively, and further worked up for proteomic analysis using the SWATH
      technique. Enzymatic activities of citrate synthase and the electron transfer
      chain (ETC) complexes I, II, and IV were assessed. Ultrastructural analyses were 
      performed by transmission electron microscopy. During progression to overt HF,
      intricate expression changes were mainly detected for proteins belonging to the
      tricarboxylic acid cycle, glucose and fat metabolism, and the ETC complexes, even
      though ETC complex I, II, or IV enzymatic activities were not significantly
      influenced. Treatment with a RAS-/NEP-inhibitor then reversed some maladaptive
      metabolic adaptations, positively influenced the decline of citrate synthase
      activity, and altered the composition of each respiratory chain complex, even
      though this was again not accompanied by altered ETC complex enzymatic
      activities. Finally, ultrastructural evidence pointed to a reduction of
      autophagolytic and degenerative processes with omapatrilat-treatment.
      CONCLUSIONS: This study describes complex adaptations of the mitochondrial
      proteome in experimental tachycardia-induced heart failure and shows that a
      combined RAS-/NEP-inhibition can beneficially influence mitochondrial key
      pathways.
FAU - Grois, Laura
AU  - Grois L
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Hupf, Julian
AU  - Hupf J
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Reinders, Jorg
AU  - Reinders J
AD  - Institute of Functional Genomics, University Regensburg, Regensburg, Germany.
FAU - Schroder, Josef
AU  - Schroder J
AD  - Electron Microscopy Core Facility, Institute for Pathology, University Hospital
      Regensburg, Regensburg, Germany.
FAU - Dietl, Alexander
AU  - Dietl A
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Schmid, Peter M
AU  - Schmid PM
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Jungbauer, Carsten
AU  - Jungbauer C
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Resch, Markus
AU  - Resch M
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Maier, Lars S
AU  - Maier LS
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
FAU - Luchner, Andreas
AU  - Luchner A
AD  - Department of Internal Medicine I, Clinic St. Marien, Amberg, Germany.
FAU - Birner, Christoph
AU  - Birner C
AD  - Department of Internal Medicine II, University Hospital Regensburg, Regensburg,
      Germany.
LA  - eng
PT  - Journal Article
DEP - 20170111
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC5226780
EDAT- 2017/01/12 06:00
MHDA- 2017/01/12 06:00
CRDT- 2017/01/12 06:00
PHST- 2016/04/13 [received]
PHST- 2016/12/21 [accepted]
AID - 10.1371/journal.pone.0169743 [doi]
AID - PONE-D-16-15026 [pii]
PST - epublish
SO  - PLoS One. 2017 Jan 11;12(1):e0169743. doi: 10.1371/journal.pone.0169743.
      eCollection 2017.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>