The Steinmetz Cardiomyopathy Fund

This fund established in memory of Dr. Michael Steinmetz, a pioneer in biotechnology and healthcare who died of an aggressive, inherited form of dilated cardiomyopathy (DCM).

Familial DCM is a genetic disease that occurs when the heart muscle dilates, cannot contract normally, and therefore cannot pump blood efficiently. It is one of the main causes of heart failure and the leading reason for heart transplantations.

Currently, diagnosis and management of DCM rely heavily on complex medical procedures including echocardiography, heart biopsies and genetic testing. Our mission is to find a cure for this deadly disease and help all affected families. 

Cardiomyopathy Heart Diagram

Donations

Your donation to the Steinmetz Cardiomyopathy Fund will be used to dissect the molecular and genetic mechanisms underlying DCM and accelerate the development of new personalised approaches to detect, monitor and ultimately prevent the disease in its earliest stage. Major challenges lie in establishing less cumbersome systems to monitor disease progression and determine early hallmarks of disease. The funds will be used for collaborative research led by Dr. Lars Steinmetz. 

All donations are tax-deductible in the USA and can be made via:

The Stanford University donations page

  •  Select Stanford Medicine, then Stanford Medicine (Other) from the drop-down options
  •  Type in “GHEYN- Steinmetz Cardiomyopathy Fund- IMO Michael Steinmetz”

Check to Stanford University

Please be sure to write “GHEYN- Steinmetz Cardiomyopathy Fund- IMO Michael Steinmetz” in the memo line for your funds to be deposited into the correct account:

Stanford University Development Services P.O. Box 20466 Stanford, CA 94309-0466

Research enabled by the Steinmetz Cardiomyopathy Fund:

  • AAV9-mediated TNPO3 overexpression in the heart rescues RBM20 cardiomyopathy in mice. Kornienko J, Schraft L, Fenzl K, van den Hoogenhof MMG, Steinmetz LM. Circulation (2025). DOI
  • Mislocalization of pathogenic RBM20 variants in dilated cardiomyopathy is caused by loss-of-interaction with Transportin-3. Kornienko J; Rodríguez-Martínez M; Fenzl K; Hinze F; Schraivogel D; Grosch M; Tunaj B; Lindenhofer D; Schraft L; Kueblbeck M; Smith E; Mao C; Brown E; Owens A; Saguner AM; Meder B; Parikh V; Gotthardt M; Steinmetz LM. Nature Communications (2023). DOI
  • Striated muscle-specific base editing enables correction of mutations causing dilated cardiomyopathy. Grosch M; Schraft L; Chan A; Küchenhoff L; Rapti K; Ferreira AM; Kornienko J; Li S; Radke MH; Krämer C; Clauder-Münster S; Perlas E; Backs J; Gotthardt M; Dieterich C; van den Hoogenhof MMG; Grimm D; Steinmetz LM. Nature Communications (2023). DOI
  • Cardiac splicing as a diagnostic and therapeutic target. Gotthardt M, Badillo-Lisakowski V, Parikh VN, Ashley E, Furtado M, Carmo-Fonseca M, Schudy S, Meder B, Grosch M, Steinmetz L, Crocini C, Leinwand L. Nature reviews Cardiology. (2023) DOI
  • Single-molecule, full-length transcript isoform sequencing reveals disease-associated RNA isoforms in cardiomyocytes. Zhu C, Wu J, Sun H, Briganti F, Meder B, Wei W, Steinmetz LM. Nature communications (2021). DOI
  • iPSC modeling of RBM20-deficient DCM identifies upregulation of RBM20 as a therapeutic strategy. Briganti F, Sun H, Wei W, Wu J, Zhu C, Liss M, Karakikes I, Rego S, Cipriano A, Snyder M, Meder B, Xu Z, Millat G, Gotthardt M, Mercola M, Steinmetz LM. Cell reports (2020). DOI

 

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