Pre-Conference Workshop Day

Tuesday, October 24, 2023

Coffee and Registration | 09:00

Workshop A | 09:30 – 11:30

Integrating Omics Data & Biology to Turn Data Sets into Mechanistic Understanding & Targetable Fibrosis Pathways


Recent developments in big data and omics have generated datasets across single cell RNA sequencing, spatial transcriptomics, single cell ATA sequencing, proteomics and spatial proteomics on fibrosis. From here, the challenge is integration of data sets into atlases, identifying missing datasets and incorporating insights into existing fibrosis biology understanding. Combining these datasets will uncover molecular networks, pathways and key regulatory factors involved in fibrotic progression.

• Better interrogate and profile samples from large datasets to identify variants of fibrosis susceptibility and progression
• Discuss identified cell types and proteins associated with fibrosis to understand drug targets and their downstream effects
• Strategize to more valuably turn omics data into key insights on targetable fibrotic pathways
• Use multi-omics data to find fibrotic biomarkers through assessing genetic variants, expression changes, comprehensive molecular profiling, differentially expressed proteins and metabolites
• Understand how to use learnings of omics data to improve patient stratification, selection and outcomes clinical trial design

11:30 Lunch & Networking

Workshop C | 13.30 – 15.30

Harnessing the Synergy Between Ageing & Fibrosis, & Exploring the Role of Targeting Senescence as an Antifibrotic Strategy

  • Massimo Attanasio Clinical Development for Immunology, Cardiovascular & Fibrosis, Bristol Myers Squibb


As the role of cell senescence in fibrosis is better understood, different perspectives have evolved on the value of targeting senescence as a therapeutic target. While targeting the abundant pro-fibrotic secretome presents a valuable antifibrotic tool, the possible implications of reducing the cancer-suppressing capacity of patients in targeting senescent cells must be considered. Are there modifiable senescence pathways or targetable subsets of fibroblasts that might reduce fibrosis without losing critical immunoprotected factors?

• Establishing to what degree senescent cells underly disease pathology in fibrosis
• Progressing knowledge of the interplay between macrophages and senescent cells and how this impacts cellular repair
• Understanding the ageing of progenitor cells and how this impacts disease
• Discovering less heterogenous targets that lie on the intersection between ageing and fibrosis to promote tissue repair and regeneration