Importantly, senescent cells can be proinflammatory and would perpetuate CF chronic inflammation.

Moreover, the developed strategy was successfully used to remove senescent cells in vivo.

Meanwhile, the steady accumulation of senescent cells with age also has adverse consequences.

Despite the decline in their proliferative potential, senescent cells display a high metabolic activity.

Through the use of label-free micro-Raman spectroscopy, control and senescent cells were noninvasively imaged.

We previously found genetic clearance of senescent cells from progeroid INK-ATTAC mice prevents lipodystrophy.

However, production of cytokines and growth factors by senescent cells may contribute to tumour development.

Direct analyses of mRNA and protein show that CPT1C is significantly reduced in senescent cells.

Here we show that the accumulation of senescent cells promotes hepatic fat accumulation and steatosis.

Finally, uptake is downregulated in senescent cells, making them insensitive to proliferative stimuli by growth factors.

Mechanistically, we show that mitochondria in senescent cells lose the ability to metabolize fatty acids efficiently.

Silencing S6K1 in senescent cells reduced superoxide generation and enhanced NO production.

During crisis, extensive cell death occurs and the cells exhibit some gene expression changes similar to senescent cells.

The senescent cells, in medium free of glucose and bicarbonate, showed impaired activity in migration and tube formation.

It was also found that the formation of protein corona could delay the QDs' toxicity on senescent cells.

Our study indicates targeting senescent cells or their products may alleviate age-related dysfunction of progenitors, adipose tissue, and metabolism.