A thesis opens up new avenues for combating cardiac fibrosis following a heart attack
The research new mechanisms that regulate fibroblast activation and paves the way for future therapies against fibrosis
Photo: ManuelCastells/Nerea Garitano, who holds a bachelor’s degree in Biochemistry Master's Degree research from the University of Navarra.
26 | 03 | 2026
Cardiovascular diseases remain the leading cause of death worldwide and place an enormous burden on healthcare systems, according to the World Health Organization. In this context, cardiac fibrosis is a core topic process: following a heart attack, the heart forms scar tissue that reduces its ability to contract and relax normally, which can lead to heart failure and other complications. Understanding how this process originates is essential for developing new therapeutic strategies.
Nerea Garitano (Elorrio, 28), a graduate in Biochemistry and Master's Degree research from the University of Navarra, completed her thesis the cardiovascular research group at Cima of Navarra, under the supervision of Dr. Beatriz Pelacho. Her work focused on studying the mechanisms that trigger cardiac fibrosis, a process that currently cannot be slowed or reversed with available treatments.
The research the role of cells called cardiac fibroblasts, which are responsible for forming the scar tissue that develops in the heart following a heart attack. Although this process is initially necessary to stabilize the damaged tissue, its prolonged activation promotes the accumulation of scar tissue and the progressive deterioration of the organ.
One of the objectives of the thesis been to identify the signals that cause these cells to shift from their normal function in a healthy heart to a state that promotes fibrosis. “Understanding how this change begins is essential, because you can’t stop or reverse a process without first knowing how it starts,” the researcher notes.
The work also work a significant new finding: it identifies subject that regulates the activation of cardiac fibroblasts. According to Dr. Garitano, this finding particularly interesting from a therapeutic standpoint.
“The main finding of my research that it identifies a fibroblast activation subject is more susceptible to modulation by subject ,” he explains. Furthermore, the results suggest that this pathway is not exclusive to the heart. “We have observed that it is also involved in fibrotic processes in other organs, suggesting that it may be a common pathway in various fibrotic diseases.”