ABSTRACT
First Person is a series of interviews with the first authors of a selection of papers published in Disease Models & Mechanisms, helping researchers promote themselves alongside their papers. Farah Abou Daya is first author on ‘ Identifying novel links between cardiovascular disease and insomnia by modeling genes from a pleiotropic locus’, published in DMM. Farah conducted the research described in this article while a PhD candidate in Girish Melkani's lab at The University of Alabama at Birmingham, Birmingham, AL, USA. She is now a postdoc in the lab of Richa Saxena at Massachusetts General Hospital, Boston, MA, USA, investigating the genetic connections and underlying mechanisms between cardiovascular diseases and sleep disorders.
Farah Abou Daya
Who or what inspired you to become a scientist?
I was inspired by my parents, who are both teachers, as they nurtured my curiosity and love for learning from a young age. Growing up in an environment that valued education made me naturally curious about the world around me. Also, through volunteering with the Red Cross, I saw firsthand how illness can affect people's lives, which sparked my interest in understanding how the human body functions and what happens when that function is disrupted. It motivated me to learn more about pathobiology so I could help others through science.
What is the main question or challenge in disease biology you are addressing in this paper? How did you go about investigating your question or challenge?
While existing literature shows that insomnia and cardiovascular disease are linked, we still don't fully understand the genetic mechanisms that connect them. The American Heart Association recently emphasized the importance of sleep by updating its ‘Life's Simple 7’ to ‘Essential 8’, recognizing sleep health as an important component of cardiovascular wellness. To investigate this link, we used human genetic data to identify a genetic locus associated with both insomnia and cardiovascular disease. We then used fruit fly models to study genes at this locus by altering their expression through tissue-specific knockdowns. To assess their roles in sleep and heart function, we performed sleep/activity monitoring and cardiac physiological imaging. Beyond evaluating gene effects within individual tissues, we also assessed how changes in one tissue, such as neurons, could influence another, like the heart, revealing cross-tissue interactions to better understand how sleep disruption contributes to cardiovascular dysfunction, and vice versa.
How would you explain the main findings of your paper to non-scientific family and friends?
We found that several genes located near a genetic region shared between insomnia and cardiovascular disease are required for normal sleep or heart function. When we reduced the expression of these genes in fruit flies, either in the neurons or the heart, it led to disrupted sleep or impaired heart function. We found that these disruptions were also accompanied by signs of inflammation in the respective tissue. In some cases, changes in one tissue, like neurons, led to problems in the other, like the heart, pointing to crosstalk between tissues. To test whether inflammation might be the link between sleep and heart dysfunction we found, we induced inflammation in the neurons. This not only disrupted sleep but was also enough to cause heart problems. When we did the same in the heart, it not only impaired cardiac function but also disturbed sleep. These results suggest that inflammation is a key mechanism connecting sleep and cardiac dysfunction.
Our findings not only uncover how sleep and heart function are biologically related, but also offer a framework for rethinking how we approach each condition in the clinic.
What are the potential implications of these results for disease biology and the possible impact on patients?
Our findings not only uncover how sleep and heart function are biologically related, but also offer a framework for rethinking how we approach each condition in the clinic. By identifying genetic regulators that affect both sleep and cardiac physiology, and pinpointing inflammation as a shared mechanism, we provide insight into why these diseases co-occur, and how dysfunction in one system may actively contribute to pathology in the other. Clinically, this means that sleep disorders shouldn't just be viewed as symptoms or side effects, but as potential contributors to cardiovascular risk. Similarly, cardiac dysfunction may be more than just a downstream consequence of poor sleep – it may also influence sleep quality through shared molecular pathways. Understanding this bidirectional relationship can help inform earlier and more comprehensive interventions. Moreover, our identification of inflammation as a connecting mechanism provides a tangible target. Therapies aimed at reducing systemic or localized inflammation may help alleviate symptoms in both domains, or even prevent disease progression altogether. This opens the door to dual-purpose treatments, as well as screening strategies that consider sleep and cardiovascular health together, rather than in isolation. Our work contributes to a more integrated model of disease biology, one in which the nervous and cardiovascular systems are viewed as interconnected players in chronic disease. This could drive the development of more effective and personalized approaches for clinical care.
Knockdown of Lsn, a gene near a cardiovascular disease- and insomnia-related locus, in the heart results in significant dilation and fibrosis.
Knockdown of Lsn, a gene near a cardiovascular disease- and insomnia-related locus, in the heart results in significant dilation and fibrosis.
Why did you choose DMM for your paper?
We chose DMM because the journal has a strong reputation for highlighting research that bridges basic biological discoveries with relevance to human disease. Our study uses a genetic model organism to explore the functional links between two major health conditions, insomnia and cardiovascular disease, and identifies conserved genes and inflammatory pathways that may drive both. DMM's focus on using model systems to understand disease mechanisms made it an ideal fit for our work, especially as our findings have both mechanistic depth and translational relevance. Since DMM highlights studies that use model organisms to uncover disease mechanisms, it felt like the perfect place for our work, especially as our findings have both mechanistic and translational insights.
Given your current role, what challenges do you face and what changes could improve the professional lives of other scientists in this role?
As a postdoc, one of the biggest challenges we face is securing stable funding. Grant writing is time consuming and often uncertain, and the pressure to constantly apply for grants can be overwhelming, especially when faced with tight deadlines and limited resources. Additionally, balancing research responsibilities with professional development and long-term career planning can be difficult. To address this, institutions and foundations could provide more consistent funding opportunities and develop more structured career development programs to better support career growth and ease the challenges of securing grants.
What's next for you?
I just started my postdoc at Massachusetts General Hospital, where I am investigating the specific role of inflammation in insomnia and how these mechanisms mediate its connection to cardiovascular disease.
Tell us something interesting about yourself that wouldn't be on your CV
I like writing short stories and have been building a growing collection since I was 15.
Farah Abou Daya's contact details: Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA 02114, USA.
E-mail: [email protected]
