Apelin gene-deficient mice developed impaired cardiac contractility with aging and pressure overload, proving apelin is essential for normal heart function and a potential therapeutic target for heart failure.
Key findingApelin knockout mice showed impaired cardiac contractility that worsened with aging and pressure overload, definitively establishing apelin as an esse
What the researchers found
Apelin knockout mice showed impaired cardiac contractility that worsened with aging and pressure overload, definitively establishing apelin as an essential cardiac peptide and a therapeutic target for heart failure and age-related cardiac decline.
Why it matters
Relevant for neuropeptides, cardiovascular.
How the study worked
animal-study study on neuropeptides, cardiovascular.
What this study cannot tell us
See abstract.
How to read the evidence
moderate evidence.
When this study was published
Published in 2007.
The bigger picture
Advances peptide research.
Questions still open
- Further research needed.
- Clinical translation to evaluate.
Common questions
What was studied?
What was found?
Read the original research
Impaired heart contractility in Apelin gene-deficient mice associated with aging and pressure overload.
Circulation research, 101(4), e32-42
Citation
Kuba, Keiji; Zhang, Liyong; Imai, Yumiko; Arab, Sara; Chen, Manyin; Maekawa, Yuichiro; Leschnik, Michael; Leibbrandt, Andreas; Markovic, Mato; Schwaighofer, Julia; Beetz, Nadine; Musialek, Renata; Neely, G Greg; Komnenovic, Vukoslav; Kolm, Ursula; Metzler, Bernhard; Ricci, Romeo; Hara, Hiromitsu; Meixner, Arabella; Nghiem, Mai; Chen, Xin; Dawood, Fayez; Wong, Kit Man; Sarao, Renu; Cukerman, Eva; Kimura, Akinori; Hein, Lutz; Thalhammer, Johann; Liu, Peter P; Penninger, Josef M. (2007). Impaired heart contractility in Apelin gene-deficient mice associated with aging and pressure overload.. Circulation research, 101(4), e32-42.