Sodium-ion channels are proteins that transmit electrical charges into electrically excitable cells, such as heart or brain cells, via their outer membranes. These channels in the heart tell muscle cells when to contract and pass the information on. This allows the organ to pump blood as a unified unit. However, damaged heart cells often lose all or part of their ability to convey these signals and join the effort, whether due to disease or trauma.
Researchers have demonstrated a gene therapy in live mice that helps heart muscle cells electrically activate. The first of its kind method could likely advance Cell & Gene Therapy Manufacturing Services Market as electrically stimulating heart cells in live mammals could lead to new gene therapy treatments for various heart diseases.
The novel method uses altered bacterial genes that code for sodium ion channels. It is the first of its type and could lead to a therapy for many electrical heart illnesses and disorders.
The method used to deliver genes in mouse heart muscle cells has persisted for a long time. The research suggests that it could effectively help hearts that don't beat as regularly as they should. Researchers improved heart muscle cells initiation and spread electrical activity, which is difficult to achieve with drugs or other tools.
These forms of transported genes, according to scientists, produce proteins while floating freely within the cell, utilizing the cell's biochemical machinery. According to previous research using this viral gene delivery method, the transplanted genes should remain active for many years. This kind of gene therapy adds more genes to a cell. It does not seek to remove, alter, or modify the existing DNA in any manner.
Tests on cells in a lab setting imply that the treatment increases electrical excitability sufficiently to prevent human disorders such as cardiac arrhythmias as proof of concept. The findings show that sodium ion channels are active in the hearts of live mice, with trends toward improved excitability. However, additional investigation is required to evaluate how much difference is produced on a whole-heart basis. Further, it needs to be seen whether it is sufficient to restore electrical function in damaged or diseased cardiac tissue to be employed as a viable treatment.
In preliminary benchtop testing, the researchers identified various bacterial sodium channel genes that operate better. The team is also testing the efficacy of these genes to restore cardiac function in mice models of human heart disease.