Senescence and apoptosis: dueling or complementary cell fates?

In response to a variety of stresses, mammalian cells undergo a persistent proliferative arrest known as cellular senescence. Many senescence-inducing stressors are potentially oncogenic, strengthening the notion that senescence evolved alongside apoptosis to suppress tumorigenesis. In contrast to apoptosis, senescent cells are stably viable and have the potential to influence neighboring cells through secreted soluble factors, which are collectively known as the senescence-associated secretory phenotype (SASP). However, the SASP has been associated with structural and functional tissue and organ deterioration and may even have tumor-promoting effects, raising the interesting evolutionary question of why apoptosis failed to outcompete senescence as a superior cell fate option. Here, we discuss the advantages that the senescence program may have over apoptosis as a tumor protective mechanism, as well as non-neoplastic functions that may have contributed to its evolution. We also review emerging evidence for the idea that senescent cells are present transiently early in life and are largely beneficial for development, regeneration and homeostasis, and only in advanced age do senescent cells accumulate to an organism's detriment

COVID-19 and cellular senescence

The clinical severity of coronavirus disease 2019 (COVID-19) is largely determined by host factors. Recent advances point to cellular senescence, an ageing-related switch in cellular state, as a critical regulator of SARS-CoV-2-evoked hyperinflammation. SARS-CoV-2, like other viruses, can induce senescence and exacerbates the senescence-associated secretory phenotype (SASP), which is comprised largely of pro-inflammatory, extracellular matrix-degrading, complement-activating and pro-coagulatory factors secreted by senescent cells. These effects are enhanced in elderly individuals who have an increased proportion of pre-existing senescent cells in their tissues. SASP factors can contribute to a 'cytokine storm', tissue-destructive immune cell infiltration, endothelialitis (endotheliitis), fibrosis and microthrombosis. SASP-driven spreading of cellular senescence uncouples tissue injury from direct SARS-CoV-2-inflicted cellular damage in a paracrine fashion and can further amplify the SASP by increasing the burden of senescent cells. Preclinical and early clinical studies indicate that targeted elimination of senescent cells may offer a novel therapeutic opportunity to attenuate clinical deterioration in COVID-19 and improve resilience following infection with SARS-CoV-2 or other pathogens

Crystallization of 2H and 4H PbI2in Carbon Nanotubes of Varying Diameters and Morphologies.

The crystallization of the complex halide PbI2 in discrete and bundled single-walled carbon nanotubes (SWNTs), double-walled carbon nanotubes (DWNTs), and thicker walled nanotubes is described. The nanotubes were produced by either arc synthesis or catalytic chemical vapor deposition. The obtained crystals could be described in terms of 1D fragments derived principally from the 2H form of PbI2, although some evidence for the formation of fragments derived from 4H PbI2 in some nanotubes was observed. The crystallization inside nanotubes was compared to the crystallization behavior of bulk PbI2 as determined by X-ray powder diffraction measurements obtained under comparable heating conditions. While the 2H to 4H polytype transition is clearly observable in bulk PbI2, stacking behavior correlated with this type of polytypism was only very occasionally observed within nanotubes, suggesting that crystallizing PbI2 within nanotubes has a tendency to order the halide into the 2H form. Additionally, PbI2 apparently does not crystallize in rigid narrow DWNTs with internal diameters of less than 2 nm. Raman studies performed on the PbI2-filled nanotubes show that the ratio of intensity of the D and G bands generally increases after filling and that both the RBM peaks and the G band are slightly upshifted