A thesis opens up new avenues for combating cardiac fibrosis following a heart attack

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.”

framework research, the team worked with a drug that acts on these cellular mechanisms. The results show that this compound is capable of reversing fibrosis in various organs, including the heart, lungs, and skin. “We have also observed these effects in patient samples, which reinforces its potential clinical applicability,” Garitano emphasizes.

Although this is still research , the results pave the way for development antifibrotic treatments. The next step will be to move toward models that more closely resemble internship . “The goal for this knowledge to remain confined to the laboratory, but rather to be translated into treatments capable of slowing or reversing fibrosis,” the researcher concludes.

reference letter
· Aguado-Alvaro LP, Garitano N, Esser-Skala W, Sayers J, Del Valle C, Alameda D, Mendieta-Esteban J, Calleja-Cervantes ME, Goñi-Salaverri A, Zazpe J, de Vito AR, Marchese F, Alignani D, Cudini J, Gross T, Rábago G, Narayan N, Martinez L, Martinez S, Huntly B, Riley P, Gonzalez A, Taylor-King JP, Fortelny N, Pelacho B, Lara-Astiaso D. Identification of epigenetic regulators of fibrotic transformation in cardiac fibroblasts through bulk and single-cell CRISPR screens. Nat Commun. 2025 Nov 26;16(1):11660. doi: 10.1038/s41467-025-66597-9. PMID: 41298482; PMCID: PMC12749234.