Unveiling the transcriptional and cellular landscape of age across human tissues

Document typeConference report
Defense date2021-05
PublisherBarcelona Supercomputing Center
Rights accessOpen Access
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Abstract
As the aging population grows progressively around the
globe, the need to research and develop strategies to healthy
aging is ever more critical and takes on new urgency1.
Primary hallmarks of aging include cell autonomous changes
linked to epigenetic alterations, genomic instability, telomere
attrition and loss of proteostasis (protein homeostasis), which
are followed by antagonistic responses such as deregulated
nutrient sensing, altered mitochondrial function and cellular
senescence. In addition, many functions of the immune system
show a progressive decline with age, referred as
immunosenescence, leading to a higher risk of infection,
cancer, and autoimmune diseases2. Although chronological
age is the most powerful risk factor for most chronic diseases,
the underlying molecular mechanisms that lead to generalized
disease susceptibility are largely unknown.
In recent years, rapidly developing high-throughput omics
have provided a broader insight, with the identification of a
number of longevity-relevant loci based on genome-wide
association studies (GWAS) and epigenome analyses. Despite
this success, APOE, FOXO3 and 5q33.3 are the only
identified loci consistently associated with longevity3. Hence,
the complexity of the aging phenomenon, influenced by
genetic and epigenetic regulation, post-translational regulation,
metabolic regulation, host–microbiome interactions, lifestyle,
and many other elements, primarily explains the poor
understanding of many of the molecular and cellular processes
that underlie the progressive loss of healthy physiology.
CitationRipoll-Cladellas, A.; G.P. van der Wijst, M.; Melé, M. Unveiling the transcriptional and cellular landscape of age across human tissues. A: . Barcelona Supercomputing Center, 2021, p. 65-66.
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