Proteomics Research Blog

Marfan Syndrome: Decoding Aortic Risk from Fibrillin Mutation to Precision Medicine

Authors: Katharina Schatz, Ronny Schmidt, Monique Eutebach

Marfan Syndrome is a hereditary connective tissue disorder and a leading genetic cause of thoracic aortic aneurysm and dissection. Once considered primarily a structural disease, it is now recognised as a complex molecular signalling disorder driven by dysregulated TGF-β pathways, extracellular matrix remodelling and oxidative stress.

Explore how emerging biomarkers, together with high-throughput proteomics and antibody microarrays, are enabling molecular risk stratification and advancing Precision Medicine in Marfan Syndrome.

Infographic illustrating the molecular pathogenesis and systemic manifestations of Marfan syndrome, showing FBN1 mutation, defective fibrillin-1, increased TGF-β signalling, extracellular matrix degradation, and major clinical features including aortic aneurysm, lens dislocation and skeletal abnormalities.

Molecular mechanisms and systemic manifestations of Marfan Syndrome: FBN1 mutations lead to defective fibrillin-1, dysregulated TGF-β signalling and extracellular matrix breakdown, driving aortic aneurysm formation and multisystem involvement affecting the cardiovascular, ocular, musculoskeletal and pulmonary systems.

Stay tuned!

Sciomics Protomics Research Blog

At Sciomics, we are dedicated to advancing healthcare through proteomics research.
We are collaborating with research groups and big pharma, alongside our in-house biomarker research initiatives.
To make this research more accessible to you, we launched the Sciomics science blog!

Decoding Protein Complexity: The Fundamental Role of Post-Translational Modifications in Cellular Function and Disease

Authors: Henning Boekhoff, Jana S. Röder

Proteins are key players in cellular functions. They are encoded by their corresponding genes, but protein functions and activity are remarkably diverse and dynamic, largely due to post-translational modifications (PTMs). PTMs are covalent chemical changes to the side chains of amino acids that occur after protein synthesis, enhancing protein diversity across life forms from Archaea to Eukaryotes. This mechanism complements the complex network of proteomic regulation, greatly expanding upon gene expression, gene duplication, and alternative splicing. While the genome acts as a blueprint, providing the necessary information to build a functioning cell, the proteome is a complex structure that vastly extends beyond the blueprint’s scope.

Protein functions and activity are remarkably diverse and dynamic, largely due to post-translational modifications (PTMs). PTMs are covalent chemical changes to the side chains of amino acids that occur after protein synthesis, enhancing protein diversity across life forms from Archaea to Eukaryotes. This mechanism complements the complex network of proteomic regulation, greatly expanding upon gene expression, gene duplication, and alternative splicing.

The Parkinson’s Revolution: How Proteomics and Biomarkers Transform Diagnosis and Development of Disease-Modifying Therapies

Authors: Ronny Schmidt, Monique Eutebach

Parkinson’s Disease remains one of the most complex neurodegenerative disorders, driven by diverse molecular mechanisms and marked heterogeneity across patients. In this article, we explore how advances in proteomics and biomarker research are reshaping our understanding of this α-Synuclein pathology, improving diagnostic accuracy, and accelerating the development of disease-modifying therapies. Discover how Precision Medicine, molecular stratification, and innovative analytical technologies are paving the way toward earlier detection and truly targeted interventions in Parkinson’s Disease.

Key molecular and cellular hallmarks of Parkinson’s Disease reflect the multifactorial nature of neurodegeneration. α-Synuclein aggregation, neuroinflammation, mitochondrial dysfunction, oxidative stress, impaired proteostasis, and gut–brain axis involvement drive disease progression and define critical targets for biomarker discovery and precision therapy development.

Key molecular and cellular hallmarks of Parkinson’s Disease reflect the multifactorial nature of neurodegeneration: α-Synuclein aggregation, neuroinflammation, mitochondrial dysfunction, oxidative stress, impaired proteostasis, and gut–brain axis involvement drive disease progression and define critical targets for biomarker discovery and precision therapy development.

Biomarker Discovery for Predicting Dengue Deterioration: A Breakthrough Study

Authors: Jana S. Röder, Henning Boekhoff

Dengue is caused by the dengue virus (DENV), which is transmitted by multiple Aedes mosquito species. The disease has spread globally due to globalization, but infections are currently most common in tropical and subtropical regions. Endemic transmission of the dengue virus is mainly reported in the Eastern Mediterranean, the Americas, Southeast Asia, the Western Pacific, and Africa. However, transmissions have also been reported in Europe and the United States. In 2023, the World Health Organization (WHO) reported a near historic peak of dengue cases: there were over five million cases and more than 5000 dengue-related deaths. Close to 80 % of these cases, or 4.1 million, have been reported in the region of the Americas. The WHO states that the actual disease burden is likely higher, due to under-reporting of infections. It is estimated that more than half of the world’s population lives in areas affected by dengue virus. Dengue is a global threat.

Dengue is a disease caused by dengue virus (DENV), which is transmitted by Aedes species. Dengue is a global threat. Simple and inexpensive strategies for the identification of patients with severe or life-threatening illness are urgently needed.