Research Areas

The Suda Laboratory investigates how cellular senescence contributes to aging-related disease, with a focus on senescent-cell heterogeneity, cardiovascular and metabolic dysfunction, and the development of senotherapeutics and biomarkers for clinical translation.

Cellular senescence is a heterogeneous process that varies across cell types and disease contexts. In a 2025 Cell Metabolism study, cell-type-specific senescent-cell elimination models (p16-Lox-ATTAC) were used to investigate the contribution of senescent endothelial cells to metabolic dysfunction. Selective removal of p16-positive senescent endothelial cells attenuated inflammatory signaling and improved metabolic dysfunction in obese mice. Conversely, transplantation of senescent endothelial cells into lean mice induced adipose tissue inflammation and metabolic dysfunction. These findings identify senescent endothelial cells as a potential therapeutic target for metabolic disease.

Not all senescent cells respond equally to senolytic treatment. A 2026 Aging Cell study characterized inflammatory senolytic-sensitive senescent cells and low inflammatory senolytic-resistant senescent cells. The study further identified a potential sensitizing to senolytics (Senosensitizer) by amplifying inflammatory signaling. This could be a novel therapeutic strategy for cancer treatment in which senosensitizers prime anticancer therapy-resistant cancer cells for senolysis, rendering them susceptible to senolytic agents and enabling their selective elimination.

A 2021 Nature Aging study identified GPNMB as a surface antigen enriched in senescent vascular endothelial cells and developed a vaccine-based senolytic strategy targeting GPNMB-positive cells. Senolytic vaccination reduced the abundance of GPNMB-positive cells, improved adipose tissue inflammation and systemic metabolic abnormalities, reduced atherosclerotic burden and improved age-associated phenotypes. The intervention also extended lifespan in a progeroid mouse model.

A 2024 Nature Aging study identified SGLT2 inhibition as an indirect senolytic strategy. Treatment with the SGLT2 inhibitor reduced senescent-cell burden in visceral adipose tissue and improved adipose tissue inflammation and metabolic dysfunction in obese mice and extended lifespan in a premature-aging mouse model. Mechanistically, SGLT2 inhibition enhanced endogenous immune-mediated clearance of senescent cells through metabolic remodeling and downregulation of the immune-checkpoint molecule PD-L1.

The Translational Geroscience Network (TGN) is a national collaborative infrastructure designed to accelerate the translation of interventions that target fundamental mechanisms of aging into human clinical trials. The Facility for Geroscience Analysis (FGA) serves as an analytical laboratory within TGN. FGA develops, validates and provides assays for biomarkers of fundamental aging processes, target engagement and gerotherapeutic response.

At Cedars-Sinai, the Center for Advanced Gerotherapeutics serves as a central hub within the TGN and plays a leading role in the FGA. Through these collaborative and analytical platforms, the Center supports identifying biomarkers that can assess biological aging and monitor the effects of gerotherapeutic interventions in humans. This work helps translate advances in the biology of aging into therapeutic strategies for age-related diseases.