New Hope for Heart Failure Patients

There are over 1000 scientific studies that show the relationship between reduced Ca2+ATPase and heart failure. 

The bad news: Failing hearts have 58% less Ca2+ATPase than normal hearts.[1]

The good news: Scientists are searching for ways to increase Ca2+ATPase to treat heart disease.

  • Istaroxime a recently approved cardiac drug stimulates Ca2+ATPase in the heart which promotes normal heart function in patients with heart failure.[2]
  • Researchers at the Yamaguchi University School of Medicine in Japan recently identified a compound that stimulates Ca2+ATPase in human cardiac muscle cells and improves heart function in rat studies.[3]
  • New laboratory and clinical evidence suggest that Ca2+ATPase gene therapy is beneficial for those dealing with heart failure.
  • Human trials both have shown extraordinary promise (82% risk reduction in worsening heart failure), but have yet to be replicated successfully in large trials. Stay tuned![4]

What does Ca2+ATPase have to do with the heart anyway?

The heart is a muscle, and just like any other muscle, it contracts and relaxes (just like your bicep).

A heart beat consists of a two distinct stages:

Contraction: To pump blood out of the heart
Relaxation:  To fill the heart with blood

So what is the Ca2+ATPase connection?  No surprise it comes down to calcium!  In order for the heart to contract, the level of calcium within the cells needs to rise. In order for the heart to relax, the level of calcium within the cells needs to fall. See below:


Ca2+ATPase is the worker bee responsible for making this process happen.  After the heart contracts, Ca2+ATPase clears the excess calcium out of the heart muscle cells by pumping it into storage vesicles inside the cell. The heart can relax because calcium levels are reduced.  If there is not enough Ca2+ATPase, the heart muscle no longer works efficiently. In response, the body tries to compensate by increasing the size of the heart muscle, but ultimately this backfires and heart failure occurs.




[1] Hayward C, Banner N, Morley-Smith A, Lyon A, Harding S. The current and future landscape of SERCA gene therapy for hear failure: a clinical perspective. Human Gene Therapy 26:293-304 (May 2015)

[2] DiPaola NR, Sweet WE, Stull LB, Francis GS, Schomisch Moravec C. Beta-adrenergic receptors and calcium cycling proteins in non-failing, hypertrophied and failing human hearts: transition from hypertrophy to failure. J Mol Cell Cardiol. 2001 Jun; 33(6):1283-95

[3] Ferrandi M, Barassi P, Tadini-Buoninsegni F, Bartolommei G, Molinari I, Tripodi MG, Reina C, Moncelli MR, Bianchi G, Ferrari P. Istaroxime stimulates SERCA2a and accelerates calcium cycling in heart failure by relieving phospholamban inhibition. Br J Pharmacol. 2013 Aug;169(8):1849-61.

[4] Kaneko M, Yamamoto H, Sakai H, Kamada Y, Tanaka T, Fujiwara S, Yamamoto S, Takahagi H, Igawa H, Kasai S, Noda M, Inui M, Nishimoto T. A pyridone derivative activates SERCA2a by attenuating the inhibitory effect of phospholamban. Eur JPharmacol. 2017 Nov 5;814:1-8