Max Planck Institute for Heart and Lung Research

On Sunday, March 30, 2025, the clocks in Germany will spring forward for daylight saving time. As we all adjust our watches, phones, and computers, what does this shift really do to our bodies? Experts from three different Max Planck Institutes shed light on this question.

GPRC5B binds to the Prostaglandin Receptor and affects the immune response

Utrophin increase in muscle cells normalises cell function in Duchenne muscular dystrophy

The hormone triggers insulin resistance in blood vessel endothelium in obesity

An enzyme called Ubiquitin-specific peptidase 5 is a key factor in protein quality in heart muscle cells

Scientists from 100 countries of the world work at the Max Planck Institutes. Here they write about their personal experiences and impressions. Mohamed El-Brolosy from Cairo is a doctoral student at the Max Planck Institute for Heart and Lung Research in Bad Nauheim. He talks about the cultural and structural differences between Germany and Egypt, explains the bureaucratic obstacles that can hinder research in Egypt, and describes how karate is helping him improve his German.

Newts possess the almost magical ability to regenerate damaged tissue, making them unique among vertebrates. Thomas Braun of the Max Planck Institute for Heart and Lung Research in Bad Nauheim is studying the amphibians to learn how an organism can regrow entire organs. Perhaps one day it will help enhance the capacity for regeneration in humans.

The advances made by Werner Seeger and his team in the treatment of pulmonary hypertension mean that many patients at least live longer, with a better quality of life.

The majority of the approximately six million patients in Germany who suffer from type 2 diabetes are overweight. In these patients, the effect of insulin is reduced. The cause for this insulin resistance was for a long time primarily sought in metabolic organs. We have now been able to show that insulin effects on the inner layer of blood vessels (endothelium) are important for insulin resistance in adipose tissue and muscles. The key molecule here is the hormone adrenomedullin. The results of this study may be the basis for new therapeutic approaches to treat type 2 diabetes.

The health of the cardiovascular system depends on its ability to respond appropriately to environmental conditions. Heart disease is increasingly associated with advanced age and impaired NAD+ metabolism, both conditions that correlate with defective/altered function of circadian rhythms. Our research into the role of NAD+ in the regulation of circadian rhythms in the ageing heart opens up new avenues for therapies for age-related heart disease.

How do behavior and environment influence genome function? We are interested in the epigenetic regulation of complex physiological and pathological phenotypes across generations. Epigenetic changes, which include proteins, RNAs, or chemical modifications to histones, RNAs, or DNA, are reversible. They do not alter the DNA sequence. They can change the way DNA sequences are read. Our laboratory combines bioinformatics, epigenomics, tumor biology, and fly genetics to identify and study the role of epigenetic modifications and their regulatory enzymes in aging, development, and disease.

An important part of the immune defense is the migration of leukocytes to the site of the inflammatory stimulus. This is mediated by chemical messengers whose counterparts are receptors on the surface of immune cells. Our Team from the ”G-protein signalling group” has now explored the role of a G protein-coupled receptor called P2Y10 in CD4 T cells. Mice lacking this receptor show less pronounced autoimmune responses in experiments. The study shows that P2Y10 may play a role in neurodegenerative diseases such as multiple sclerosis or other autoimmune diseases. 

Transcription factors are key regulators of complex genetic programs such as cell maturation, differentiation, or proliferation. Due to their central role, the identification of transcription factor binding positions is crucial to understand and predict cellular fate decisions. We have developed a computational method that utilizes a chromatin-accessibility assay to survey which transcription factors are active, and which genes they activate. This approach aims to unravel transcription factors dynamics and networks.