Linna Lab

Our research focuses on understanding the molecular and environmental mechanisms underlying cardiovascular aging and disease, with particular emphasis on how cellular aging and environmental exposures influence cardiac tissue vulnerability, disease progression, and therapeutic responses.

One of our key research directions is Aging Clock, a project that develops cell-type-specific biological aging clocks for the human heart using artificial intelligence (AI) and machine learning applied to large-scale single-cell transcriptomics data. Rather than treating aging as a uniform process, we quantify biological age across individual cardiac cell populations to identify cell types exhibiting accelerated or altered aging in cardiovascular disease. By integrating transcriptomics with genomics, proteomics, and metabolomics, we aim to uncover the molecular mechanisms driving these changes and identify novel therapeutic targets. This approach establishes biological aging as a quantitative phenotype for cardiovascular target discovery. Candidate mechanisms are subsequently investigated in human cardiovascular models, connecting AI-driven discoveries with experimental validation and future therapeutic interventions.

In parallel, we investigate the accumulation and biological effects of plastics in human cardiac tissue. Recent studies have demonstrated the presence of microplastics and nanoplastics in human tissues, raising concerns about their potential contribution to cardiovascular disease. Particularly concerning is emerging evidence suggesting that plastic accumulation may be associated with environmental exposure, tissue pathology, and adverse clinical outcomes. Our research examines how plastics interact with cardiac cells and their surrounding tissue environment, and whether these interactions contribute to cardiovascular disease development and progression.

We propose a “sand in a sock” paradigm, in which healthy cardiac tissue may initially tolerate accumulated plastics through adaptive cellular responses. However, during aging, injury, or disease, changes in the tissue microenvironment may disrupt this balance, increasing susceptibility to plastic-associated damage, potentially facilitating further accumulation, and amplifying existing pathological processes.

Importantly, these research directions converge on a central question: how do biological aging and environmental stressors interact to determine cardiovascular resilience and vulnerability? By combining cell-type-specific aging clocks with experimental studies of environmental exposures, we aim to investigate whether plastics contribute to accelerated biological aging in specific cardiac cell populations and whether aging-associated changes increase susceptibility to plastic-induced injury. This integrated approach provides an opportunity to identify shared molecular mechanisms, discover potential therapeutic targets, and develop new strategies for cardiovascular disease prevention.

Beyond advancing our understanding of cardiovascular disease mechanisms, our research may also provide evidence relevant to environmental health policies, with the potential to reduce harmful exposures and improve population health.

Our research is supported by University of Eastern Finland, Reseach Council of Finland, Sigrid Jusélius Foundation, Osk Huttunen Foundation, Yrjö Jahnsson Foundation, Paavo Nurmi Foundation, and Aarne Koskelo Foundation.