Christian Göritz

Erectile dysfunction (ED) is common, affecting both men and their partners, with a 66% prevalence in type 2 diabetes. Despite its impact, the underlying mechanisms of diabetes-associated ED remain poorly understood, limiting the development of effective treatments. While research has focused on vascular and neuronal factors, recent findings suggest that fibroblasts in the corpora cavernosa actively regulate norepinephrine availability and vascular tone. These fibroblasts are not static but are influenced by erectile activity, aging, and metabolic conditions. Additionally, macrophages, which regulate inflammation and tissue remodeling, may affect fibroblast function and blood flow in ED. In this project, we will investigate how fibroblast-macrophage interactions contribute to diabetes-induced ED. Using in vivo models and human penile tissue, we will assess changes in fibroblast composition, macrophage activation, and molecular signaling. Single-nucleus RNA sequencing and spatial transcriptomics will identify key ligand-receptor interactions in diabetes-associated ED. Preliminary data show that fibroblast numbers decline, while macrophage infiltration increases in ED, correlating with reduced penile blood flow. Enhanced macrophage-fibroblast signaling suggests a role in disease progression. By identifying signaling pathways driving ED, this project aims to uncover new therapeutic targets to restore erectile function and improve quality of life for men and their partners.

A tumor is a complex tissue consisting of malignant cells and the so-called stroma, which can be described as the tumor's supporting tissue. In recent years, it has become clear that the stroma of the tumor is important for its growth and spread and can therefore be an important target tissue for cancer therapy. We have recently identified several subtypes of tumor stroma and we now want to understand their importance in relation to tumor growth and spread. The project aims to find out in detail the cellular and molecular mechanisms behind the formation of the stroma and we test strategies to influence these processes and find out whether blocking the formation of the stroma affects the development of cancer. In our studies, we use an animal model for glioblastoma as well as human material from cancer patients. We suspect that mechanisms we uncover are also relevant to other solid cancer types. With our research, we hope to find new starting points for developing treatment for solid cancers, specifically glioblastoma. We intend to find out the general mechanisms behind stroma formation and try to find new targets for therapy that can prevent cancer spread.