Cardiac Remodeling

The research group investigates the cardiac remodeling processes that occur during the development of heart failure. When the heart is subjected to increased stress, for example due to valvular heart disease or following a myocardial infarction, it initially responds by adapting to the increased workload, thereby maintaining cardiovascular stability. However, under chronic stress, remodeling progressively worsens, eventually leading to a decline in cardiac function and potentially to overt heart failure.

The group’s primary objective is to understand the underlying mechanisms responsible for the transition from compensated hypertrophy (enlargement of cardiac muscle cells), with cardiac function still largely preserved, to heart failure, and to develop novel therapeutic approaches. To this end, the group conducts analyses of human cardiac tissue to gain a better understanding of the different stages of heart failure development. In parallel, modifications of mechanisms previously identified are investigated as potential therapeutic interventions using in vivo and in vitro models.

The following research areas are being investigated:

1. Impact of different forms of mechanical load on the development of heart failure: Afterload and preload have different effects on the heart (Toischer et al., 2010). Potential therapeutic interventions have been tested, including the induction of cardiomyocyte proliferation (Toischer et al., JCI, 2017), modification of ryanodine receptor leak (Mohamed et al., Science Translational Medicine, 2018), and other therapeutic targets (Khadjeh et al., Basic Research in Cardiology, 2020). Clinical investigations are conducted using biopsies from patients with severe aortic valve stenosis (Gersch et al., European Journal of Heart Failure, 2026, accepted; Gersch et al., Clinical Research in Cardiology, 2025; Xu et al., Cardiovascular Research, 2024).

2. Epigenetics in heart failure: The effects of epigenetic changes in heart failure are also being investigated, with a particular focus on N6-methyladenosine (m6A) RNA methylation (Berulava & Buchholz et al., European Journal of Heart Failure, 2019; Anamalai et al., Cell Communication and Signaling, 2025).

3. Heart–brain interaction: The heart and brain interact in various ways. In recent years, we have demonstrated that heart failure temporarily impairs cognitive function and that this effect is mediated by epigenetic mechanisms (Islam et al., EMBO Molecular Medicine, 2021; Gisa et al., Non-coding RNA, 2025).

The following projects are currently underway:

• Identification of heart failure mechanisms using human cardiac tissue samples from patients with aortic stenosis
• Differences between increased preload (e.g. aortic valve regurgitation) and increased afterload (e.g. aortic valve stenosis)
• Cardiac regeneration through cardiomyocyte proliferation
• Modulation of epigenetic mechanisms (RNA methylation, reader proteins, and microRNAs)
• Mechanisms and therapeutic strategies in heart failure with preserved ejection fraction (HFpEF)

Team

Medical Doctors

Scientific Staff

Post Doctoral

Associated Researchers (Clinical Chemistry)

PhD Students

Techical Assistant

Alumni