International Business Department           Liu Bojia           October 06, 2023

  Repairing damaged tissues is important for the survival of animals, however, for humans, it has always been a challenge to repair damaged nerves. When nerve damage occurs - for example, when nerves in the arms or legs are crushed or severed as a result of an accident - it often leads to muscle atrophy and loss of sensation, as it is very difficult for functional nerves to regenerate.

  But scientists have discovered that nerves like those in the arms and legs, which are part of the peripheral nervous system, actually have a high potential for regeneration. Under idealised experimental conditions, nerve fibres can be seen to regrow or even completely regenerate.

  However, why is it that complete recovery of nerve function remains a rare "miracle" in clinical practice? This is most likely due to the influence of Schwann cells in the peripheral nervous system.

  Schwann cells are a type of glial cell that wraps around a nerve fibre, just like the protective insulation of an electrical wire wraps around a metal conductor. When an injury occurs, the Schwann cells at the location of the damaged nerve do not die, but undergo adaptive cellular reprogramming to become repair cells responsible for coordinating the disassembly and debris removal of the damaged nerve fibre, then directing axon regeneration to provide nutrient support, and ultimately, once again, the protective wrapping of the nerve fibre.

  Predictably, Schwann cells bear a huge metabolic burden in this process. Recently, scientists at the University of Leipzig in Germany found that Schwann cells, which repair nerves, are in great need of support from fat cells.

  Using experimental mice to construct a model of acute peripheral nerve injury, they found that Schwann cells responded to the weeks-long repair process with a marked expansion of mitochondria, implying that the cells' energy metabolism was being challenged. And further tracing the pathways involved in the regulation of cellular metabolism, the researchers found that leptin, secreted by adipocytes, is key to activating mitochondria.

  Leptin is produced primarily by cells in adipose tissue and is best known for its role in suppressing appetite to prevent overeating. However, new research has found that as a chemical messenger, leptin is also an important factor influencing Schwann cells to repair damaged nerves.

  The researchers found that Schwann cells have a receptor that receives leptin signals, and it is only when this receptor is activated that Schwann cells are prompted to adaptively adjust their metabolism in order to meet the high metabolic demands required for nerve repair.

  Understanding the relationship between adipocytes and Schwann cells, the researchers suggest that regulating the metabolism of Schwann cells to provide sufficient energy for nerve repair in the case of nerve injury may be a promising therapeutic idea. It is hoped that these new findings will soon be translated into ways to promote nerve repair and regeneration in humans.