Context-dependent roles of cellular senescence in normal, aged, and disease states.

Cellular senescence is a state of irreversible cell cycle arrest that often emerges after tissue damage and in age-related diseases. Through the production of a multicomponent secretory phenotype (SASP), senescent cells can impact the regeneration and function of tissues. However, the effects of senescent cells and their SASP are very heterogeneous and depend on the tissue environment and type as well as the duration of injury, the degree of persistence of senescent cells and the organism's age.

Methods for in vivo studies in rodents of chemotherapy induced peripheral neuropathy.

Peripheral neuropathy is one of the most common, dose limiting, and long-lasting disabling adverse events of chemotherapy treatment. Unfortunately, no treatment has proven efficacy to prevent this adverse effect in patients or improve the nerve regeneration, once it is established. Experimental models, particularly using rats and mice, are useful to investigate the mechanisms related to axonal or neuronal degeneration and target loss of function induced by neurotoxic drugs, as well as to test new strategies to prevent the development of neuropathy and to improve functional restitution.

Minocycline Does Not Reduce the Regenerative Capacity of Peripheral Motor and Sensory Neurons after a Conditioning Injury in Mice.

Minocycline has been reported to be both beneficial and detrimental for nerve regeneration after peripheral nerve injury. By reducing the inflammatory response, minocycline administration reduces pain and has neuroprotective effects, but it also inhibits Wallerian degeneration in the distal stump, and reduces microglia and macrophages activity on motor and sensory neurons, which could reduce their intrinsic regenerative capacity. The aim of this study was to determine if the administration of minocycline after nerve injury inhibits the regenerative capacity of motoneurons and sensory neurons after a conditioning lesion.