Differential expression analysis in single-cell transcriptomics enables the dissection of cell-type-specific responses to perturbations such as disease, trauma, or experimental manipulations. While many statistical methods are available to identify differentially expressed genes, the principles that distinguish these methods and their performance remain unclear. Here, we show that the relative performance of these methods is contingent on their ability to account for variation between biological replicates. Methods that ignore this inevitable variation are biased and prone to false discoveries. Indeed, the most widely used methods can discover hundreds of differentially expressed genes in the absence of biological differences. To exemplify these principles, we exposed true and false discoveries of differentially expressed genes in the injured mouse spinal cord.

/pdf/confronting-false-discoveries-in-single-cell-differential-1ee3ckmt7v.pdf

Confronting false discoveries in single-cell differential expression.

Aging is characterized by systemic chronic inflammation, which is accompanied by cellular senescence, immunosenescence, organ dysfunction, and age-related diseases. Given the multidimensional complexity of aging, there is an urgent need for a systematic organization of inflammaging through dimensionality reduction. Factors secreted by senescent cells, known as the senescence-associated secretory phenotype (SASP), promote chronic inflammation and can induce senescence in normal cells. At the same time, chronic inflammation accelerates the senescence of immune cells, resulting in weakened immune function and an inability to clear senescent cells and inflammatory factors, which creates a vicious cycle of inflammation and senescence. Persistently elevated inflammation levels in organs such as the bone marrow, liver, and lungs cannot be eliminated in time, leading to organ damage and aging-related diseases. Therefore, inflammation has been recognized as an endogenous factor in aging, and the elimination of inflammation could be a potential strategy for anti-aging. Here we discuss inflammaging at the molecular, cellular, organ, and disease levels, and review current aging models, the implications of cutting-edge single cell technologies, as well as anti-aging strategies. Since preventing and alleviating aging-related diseases and improving the overall quality of life are the ultimate goals of aging research, our review highlights the critical features and potential mechanisms of inflammation and aging, along with the latest developments and future directions in aging research, providing a theoretical foundation for novel and practical anti-aging strategies. 

https://www.nature.com/articles/s41392-023-01502-8.pdf

Inflammation and aging: signaling pathways and intervention therapies

Caloric Restriction Reprograms the Single-Cell Transcriptional Landscape of Rattus Norvegicus Aging.

Age-associated changes in immune cells have been linked to an increased risk for infection. However, a global and detailed characterization of the changes that human circulating immune cells undergo with age is lacking. Here, we combined scRNA-seq, mass cytometry and scATAC-seq to compare immune cell types in peripheral blood collected from young and old subjects and patients with COVID-19. We found that the immune cell landscape was reprogrammed with age and was characterized by T cell polarization from naive and memory cells to effector, cytotoxic, exhausted and regulatory cells, along with increased late natural killer cells, age-associated B cells, inflammatory monocytes and age-associated dendritic cells. In addition, the expression of genes, which were implicated in coronavirus susceptibility, was upregulated in a cell subtype-specific manner with age. Notably, COVID-19 promoted age-induced immune cell polarization and gene expression related to inflammation and cellular senescence. Therefore, these findings suggest that a dysregulated immune system and increased gene expression associated with SARS-CoV-2 susceptibility may at least partially account for COVID-19 vulnerability in the elderly.

/pdf/a-human-circulating-immune-cell-landscape-in-aging-and-covid-2uze0na4kl.pdf

A human circulating immune cell landscape in aging and COVID-19.

Coronavirus disease-19 and fertility: viral host entry protein expression in male and female reproductive tissues.

Single-Cell Transcriptomic Atlas of Primate Ovarian Aging.

Organismal ageing results from interlinked molecular changes in multiple organs over time. The study of ageing at the molecular level is complicated by varying decay characteristics and kinetics-both between and within organs-driven by intrinsic and extracellular factors. Emerging single-cell omics methods allow for molecular and spatial profiling of cells, and probing of regulatory states and cell-fate determination, thus providing promising tools for unravelling the heterogeneous process of ageing and making it amenable to intervention. These new strategies are enabled by advances in genomic, epigenomic and transcriptomic technologies. Combined with methods for proteome and metabolome analysis, single-cell techniques provide multidimensional, integrated data with unprecedented detail and throughput. Here, we provide an overview of the current state, and perspectives on the future, of this emerging field. We discuss how single-cell approaches can advance understanding of mechanisms underlying organismal ageing and aid in the development of interventions for ageing and ageing-associated diseases.

Single-cell omics in ageing: a young and growing field.

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Single-Cell Transcriptomic Atlas of Primate Ovarian Aging.

Single-cell omics in ageing: a young and growing field.