I may have just found an article that could explain why...

I may have just found an article that could explain why bisantrene is safer for the heart than other anthracycline-based therapies.

Released 5th March, 2021, the researchers at Fudan University evaluated the FTO concentrations of peripheral blood mononuclear levels of heart failure with preserved ejection fraction (HFpEF) patients as well as HFpEF mice heart tissue (1). HFpEF accounts for 50% or higher of all heart failure cases. This number is expected to grow as the average age and waist line of people continues to grow. As discussed at lengths here, the use of anthracycline-based chemotherapeutic drugs has clearly been shown to increase the risk of heart failure. Which is further perpetuated since those who are overweight and who are older are at increased risk of being diagnosed with breast cancer or AML. It is a mess of interelated factors that increase an individuals risk of heart failure and which clearly identifies an opportunity for a safer chemotherapeutic agent. A fundamental aspect of bisantrene is the significantly reduced cardiotoxicity when compared to anthracycline-based therapies (2).

This is the “first study to explore the role of m6A methylation in HFpEF”. Other research investigating the role of FTO in heart failure has evaluated cardiomyocyte concentrations, where it was found to be downregulated (3). This article describes the mice heart as ‘heart tissue’, so I am not sure if it is measuring a cardiomyocyte or something different. Below is the abstract from the study with important points highlighted.

The study found that FTO expression is upregulated in the peripheral blood of HFpEF patients as well as in the hearts of HFpEF mice. Due to the difficulties associated with obtaining heart tissue from patients, mice hearts were used. The authors state that the altered expression patterns of m6A regulators (like FTO) in peripheral blood of “HFpEF patients represents the diagnostic potential of m6A regulators; however, the changed m6A regulators in heart tissue give inspiration to the pathological mechanisms and treatments.”

This could be the first indication of why bisantrene is a safer therapy for the heart. Further studies are needed to understand the role of FTO in the development or progression of heart failure, and whether FTO inhibition could be a potential therapy for HFpEF patients.

1. https://www.frontiersin.org/articles/10.3389/fcvm.2021.647806/full

2. https://www.raceoncology.com/wp-content/uploads/2020/08/the-rediscovery-of-bisantrene-a-review-of-the-literature-ijcrt-17-015.pdf
3. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.033794