From supporting role to the lead- story of fibroblasts

Here we are back at it again. It feels nice to write after a long, tiring week 🙂 There is a part of me that craves writing quite often, but not that articulate, boring (no offense to the lecturers) academic writing but writing as I wish from my heart.

Today’s topic is to explain why I talked about that love story about how heart muscles (cardiomyocytes) contract. Apart from being like a hopeless, romantic soap opera episode, i really hope the story i made up was quite was educational.

Following up form the story, let’s talk about how this contraction event is important in treating cardiovascular diseases. The main focus in treating heart diseases is to develop a drug to change the rate of contractiom of the heart. For instance, if a person has cardiomyopathy (to read more about cardiomyopathy-  https://www.nhs.uk/conditions/cardiomyopathy/) ; which is the weakening of the heart muscle making it hard to pump blood to the rest of the body, drugs such as beta blockers are used which act on muscle tissue in the heart to slow down the contraction rate in order to take the pressure off the heart.

All these years, cardiomyocytes had been the lead actors in this treatment story and the structural cells of the heart aka fibroblast had the supporting role :(. It has been thought that the fibroblasts in the heart can only help repair the damaged tissue by producing the proteins needed for restoration such as collagen. They are also involved in inflammation of the heart tissues. The damage in the tissues and some inflammatory molecules, cytokines, produced by immune cells to the enviroment along with other factors can activate fibroblast into myofibroblast (figure 1) to produce an enzyme called elastase which can degrade excess collagen in the environment, produce more molecules called chemokines to attract other useful cells, in addition to cytokine production. Researches did not focus on these poor cells when developing drugs to treat heart diseases as these cells did not influence contraction rate of the heart- at least that is what they thought!!!!

The important question is now; what if the structural cells can affect contraction of the heart muscles? Wouldn’t it change the whole process of developing drugs to treat cardiovascular diseases? Wouldn’t the  supporting role (fibroblast) face the possibility of becoming the lead in this story?

These questions are for you to think about for now. Hope to get back to you in 2 weeks with some answers. See you 🙂 Nermin exists once again.