Our research

We know that aging is a plastic, highly regulated process, but our understanding of the mechanisms that confer this regulation is incomplete. Detailed knowledge of these mechanisms will be crucial for any educated aging-preventive approaches. Thus the main effort of our lab is their discovery and further exploration. We conduct most of this work in the model organism Caenorhabditis elegans. This organism is ideal for aging-related research, as it is technically well established, short-lived (allowing for lifespan as an easily measurable age-related phenotype), and very responsive to alterations in its aging-regulatory pathways. Sometimes, we also use human cultured cells. The laboratory combines biochemistry (Proteomics, ChIP-Seq, ATAC-Seq, …) and transcriptomics (mRNA-Seq) with high-throughput genetic screening approaches (RNAi, forward genetics,…), to understand the regulation of aging at molecular and mechanistic resolution. Recently, we have focused on the mechanistic exploration of lifespan regulatory transcription factors, in particular DAF-16(FOXO) – a central driver of longevity that integrates many lifespan extending stimuli, i.e. nutrient deprivation, various stresses, or cues of infertility to confer transcription of a wide range of stress resistance and longevity determining genes. This work is complemented by studies on the role of chromatin states, chromatin remodelers, and the epigenome in the context of aging and age-related disease.

In this line of research, we seek pharmacological interventions against aging. For easier applicability, this work is conducted directly in mammalian systems where we validate mechanisms of particular appeal that were identified in simpler model organisms and test possible targeting strategies. Further, we develop and apply screening methodologies that allow for the identification of aging-preventive compounds in human cultured cells.

Our lab has long-standing expertise in studying how cells respond and adapt to stress. We are applying this expertise to investigate stress responses in the context of cancer. Using C. elegans, human cells, and mice, we seek new vulnerabilities that can be targeted for cancer therapy.

In collaboration with the teams of Sarah Hägg and Per Nilsson, both at Karolinska Institute, we work on the repurposing of FDA-approved drugs for treatment or prevention of Alzheimer’s disease.

Mitochondria supply cellular energy and coordinate metabolic and stress responses that influence aging. Although mitochondrial dysfunction can contribute to age-related decline, studies in C. elegans show that certain mild mitochondrial perturbations can instead activate protective programs and extend lifespan. A central question is what determines whether mitochondrial stress promotes longevity or causes damage, including its severity, timing and tissue of origin. Indeed, preserving mitochondrial function during adulthood can also extend lifespan, highlighting the importance of context. Other important questions concern how mitochondrial DNA maintenance, quality control and communication between tissues interact with other longevity pathways. Addressing these questions could reveal ways to preserve cellular function and promote healthier aging.

If you are interested in our research topics and would like to do some reading on the background, we suggest the following publications:

further reading:

Salignon, J.*, Tsiokou, M., Marqués, P., Rodríguez-Diaz, E., Ang, H., Pietrocola, F.*, Riedel, C.G.* (2026) Pasta, a Versatile Transcriptomic Clock, Maps the Chemical and Genetic Determinants of Aging and Rejuvenation. Advanced Science, e76740. (*: equal correspondence)

Kavsek, A., Salignon, J., Millan-Ariño, L, Marcinkowski, P., Sen, I., Riedel, C.G. (2025) LIN-39 is a neuron-specific developmental determinant of longevity in Caenorhabditis elegans with reduced insulin signaling. Nature Communications 16(1):6566.

Salignon, J., Faridani, O., Miliotis, T., Janssens, G.E., Chen, P., Zarrouki, B., Sandberg, R., Davidsson, P., Riedel, C.G. (2023) Age prediction from human blood plasma using proteomic and small RNA data: a comparative analysis. Aging 15.

Salignon, J., Rizzuto, D., Calderón-Larrañaga, A., Zucchelli, A., Fratiglioni, L., Riedel, C.G.*, Vetrano, D.L.* (2023) Beyond chronological age: a multidimensional approach to survival prediction in older adults. The Journals of Gerontology: Series A, Biological Sciences and Medical Sciences 78(1):158-166. (*: equal correspondence)

Janssens, G.E., Lin, X.X., Millan-Ariño, L., Sen, I., Kavšek, A., Seinstra, R.I., Stroustrup, N., Nollen, E.A.A., Riedel, C.G. (2019) Transcriptomics-based screening identifies pharmacological inhibition of Hsp90 as a means to defer aging. Cell Reports 27: 467-480.

Lin, X.X., Sen, I., Janssens, G.E., Zhou, X., Fonslow, B.R., Edgar, D., Stroustrup, N., Swoboda, P., Yates 3rd, J.R., Ruvkun, G., Riedel, C.G. (2018) DAF-16/FOXO and HLH-30/TFEB function as combinatorial transcription factors to promote stress resistance and longevity. Nature Communications 9(1): 4400.

Zhou, X., Sen, I., Lin, X.X., Riedel, C.G. (2018) Regulation of age-related decline by transcription factors and their crosstalk with the epigenome. Current Genomics, 19(6): 464-482.

Lezzerini, M., Riedel, C.G. (2016) ATP-dependent chromatin remodeling: from development to disease. Book Chapter in “Chromatin Regulation and Dynamics”, Elsevier, ISBN: 978-0-12-803395-1.

Riedel, C.G., Dowen, R.H., Lourenco, G.F., Kirienko, N.V., Heimbucher, T., West, J.A., Bowman, S.K., Kingston, R.E., Dillin, A., Asara, J.M., Ruvkun, G. (2013). DAF-16 employs the chromatin remodeler SWI/SNF to promote stress resistance and longevity. Nature Cell Biology, 15, 491-501.

López-Otín, C., Blasco, M.A., Partridge, L., Serrano, M., Kroemer, G. (2013) The hallmarks of aging. Cell 153, 1194-1217.

Feser, J., & Tyler, J. (2011) Chromatin structure as a mediator of aging. FEBS letters, 585(13), 2041–8.

Calnan, D.R. & Brunet, A. (2008) The FoxO code. Oncogene 27, 2276-88. Kenyon, C. (2005) The plasticity of aging: insights from long-lived mutants. Cell 120, 449-60.