tissues communicate with each other, exchange signals and metabolic products and influence each other. This inter-organic communication plays a decisive role in the development and treatment of diseases, but is not yet fully understood. Our metabolism in particular is closely linked to inflammatory reactions, ageing processes and chronic diseases. Metabolic products can circulate as signalling molecules between tissues to either promote healing processes or exacerbate diseases.
Inter-Organ Metabolomics: New insights for medicine
A new field of research is coming into focus: inter-organ metabolomics investigates which metabolic products are exchanged between organs, how they influence biological processes and what role they play in disease mechanisms. In order to better understand these relationships, the German Centres for Health Research (DZG) have launched the ‘Inter-Organ Metabolomics’ innovation fund. The aim is to bring together researchers from different disciplines in order to gain new insights across disciplinary boundaries.
Two outstanding projects have been selected for funding and will receive a total budget of up to 766,000 euros (project 1) and 796,000 euros (project 2) over the years 2025 and 2026.
When the immune system increases muscle loss
Muscle loss is not only the result of immobility or malnutrition - the immune system often plays a decisive role. Certain metabolic products that are released in serious illnesses such as cancer or COPD (chronic obstructive pulmonary disease) can permanently reprogramme immune cells. Instead of regulating inflammation, they drive muscle atrophy. This could play a decisive role in cachexia - a syndrome that leads to muscle loss and cannot be completely reversed even with an improved diet.
‘Our goal is to find out which metabolic products alter the immune system in such a way that it increases muscle loss. If we understand this, we can intervene therapeutically in a targeted manner,’ explains Dr Maria Rohm from Helmholtz Munich, scientist at the German Centre for Diabetes Research (DZD) and head of the funded project ’Metabolite-mediated epigenetic changes in immune cells trigger a coordinated tissue response in cachexia.’
However, not only the immune system, but also the fat metabolism could play a key role in cachexia. ‘There is evidence that adipose tissue acts as an early signalling device in cachexia and communicates with the muscles. If we can decipher these mechanisms, we may be able to slow down or even stop the process,’ says Prof Alexander Bartelt from the Technical University of Munich and scientist at the German Centre for Cardiovascular Research (DZHK).
An interdisciplinary research team from five of the eight German Centres for Health Research - DZD, DZHK, DZL (lung research), DZIF (infection research) and DKTK (translational cancer research) - is investigating these mechanisms. Using cell models, disease models and patient data, the researchers are analysing which biochemical signalling pathways control this fatal process - in the hope of developing new therapeutic approaches to combat cachexia.
"By combining metabolomics, epigenetics, and immunology, we aim to identify the mechanism of tissue communication mediated by immune cells that leads to muscle wasting in cachexia and sarcopenia," adds DZIF scientist Prof. Karsten Hiller from the Technical University of Braunschweig.
The Genetic Trail of Inflammation in Aging
Cardiovascular diseases, cancer, COPD and diabetes are among the most common age-related diseases. A genetic change in the blood system could play a central role in this: so-called ‘clonal haematopoiesis of undetermined potential (CHIP)’. It occurs in more than 20 per cent of people over the age of 65 and is associated with chronic inflammation and impaired healing processes in the heart, lungs and blood vessels.
But how exactly do these genetic changes affect the immune system and communication between the organs? The second funded project entitled ‘Targeting metabolic interorganic communication in inflammation-induced ageing - how somatic mutations drive age-related diseases’ is investigating this question.
‘We have learnt that genetic mutations in blood cells not only increase the risk of leukaemia, but also influence inflammatory and metabolic processes in other organs,’ says Prof. Michael Rieger from Frankfurt University Hospital, a scientist in the German Cancer Consortium (DKTK).
‘This finding opens up completely new possibilities for tackling age-related diseases at their root,’ adds DZL scientist Prof Soni Pullamsetti from Justus Liebig University Giessen.
The interdisciplinary research team, consisting of five of the German Centres (DKTK, DZD, DZHK, DZIF and DZL), is investigating these questions. The aim is to decipher the effects of CHIP mutations in blood cells on inflammatory processes and metabolic changes in the affected organs. These findings could make a decisive contribution to the development of new prevention and treatment strategies against age-related diseases.
DZG: Research in Collaboration Brings New Approaches
The two funded projects demonstrate that complex disease mechanisms can only be deciphered through interdisciplinary collaboration. Researchers from cardiovascular research, pulmonary medicine, oncology, metabolic medicine, and infection research are pooling their expertise to address shared questions.
The DZG Innovation Fund specifically supports collaborations across disciplines and institutions—with the goal of developing new approaches for the diagnosis and treatment of widespread diseases.
DZG Innovation Fund: Funded Projects 2025/26 on "Inter-Organ Metabolomics"
Project 1: "Metabolite-mediated epigenetic changes in immune cells induce a coordinated response across tissues in cachexia"
Participating Scientists:
Maria Rohm (DZD, Helmholtz Munich), Stephan Herzig (DZD, Helmholtz Munich), Ali Önder Yildirim (DZL, Helmholtz Munich), Soni Pullamsetti (DZL, Justus Liebig University Giessen), Karsten Hiller (DZIF, Technical University of Braunschweig), Maximilian Reichert (DKTK, TUM University Hospital), Alexander Bartelt (DZHK, Technical University of Munich)
Project 2:
"Targeting the metabolic interorgan communication of ‘inflamm-aging’—how somatic mutations drive common age-associated diseases"
Participating Scientists:
Michael Rieger (DKTK, University Hospital Frankfurt), Stefanie Dimmeler (DZHK, Goethe University Frankfurt), Soni Pullamsetti (DZL, Justus Liebig University Giessen), Triantafyllos Chavakis (DZD, Technical University of Dresden), Christoph Spinner (DZIF, Technical University of Munich)
