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SUMMARY:FGF21 signaling activation: Treating obesity at the expense of car
 diac hypertrophy? - Professor Konstantinos Drosatos (University of Cincinn
 ati College of Medicine)
DTSTART;VALUE=DATE-TIME:20251121T130000Z
DTEND;VALUE=DATE-TIME:20251121T140000Z
UID:https://talks.ox.ac.uk/talks/id/e9c27fc9-05c0-4689-bf19-16f118fca48c/
DESCRIPTION:Left ventricular hypertrophy (LVH) can occur as a physiologica
 l adaptation to transient stressors such as exercise or pregnancy\, or as 
 a pathological response to chronic strain. Pathological LVH contributes su
 bstantially to heart failure with preserved or reduced ejection fraction (
 HFpEF\, HFrEF). While intracellular drivers have been well studied\, the r
 ole of interorgan signaling remains less defined.\n\nOur recent published 
 work in humans and mice revealed a liver–brain–heart axis mediated by 
 fibroblast growth factor 21 (FGF21). Although FGF21 analogs show metabolic
  benefits and are in clinical development\, we found that under sustained 
 cardiac stress\, FGF21 can promote pathological hypertrophy. In pressure o
 verload (transverse aortic constriction\, TAC)\, hepatic FGF21 production 
 rises before cardiac dysfunction\, inducing FGF21 expression in cardiomyoc
 ytes (CMs). Subsequently\, CM-derived FGF21 disrupts hypothalamic oxytocin
  signaling\, driving pathological LVH. Deleting FGF21 from hepatocytes or 
 CMs restored oxytocin signaling and reduced LVH\, identifying CM-derived F
 GF21 as a direct mediator of cardiomyopathy.\n\nOn the other hand\, in HFp
 EF\, the effects diverged: hepatocyte-specific FGF21 deletion\, which was 
 protective in TAC\, accelerated progression to HFrEF\, suggesting an early
  adaptive role for liver-derived FGF21. Conversely\, CM-specific deletion 
 delayed HFpEF development.\n\nThese findings constitute the basis of our o
 ngoing research aiming to address how liver-derived FGF21 promotes adaptiv
 e hypertrophy\, whereas CM-derived FGF21 drives maladaptive remodeling. Th
 is work has important implications for ongoing clinical use of FGF21 analo
 gs in metabolic disease\, underscoring the need to evaluate cardiac risk a
 nd highlighting the potential of targeting the FGF21–oxytocin pathway fo
 r heart failure prevention and treatment.\n\nSPEAKER BIOGRAPHY\n\nKonstant
 inos Drosatos received his undergraduate degree in Biology from the Aristo
 tle University of Thessaloniki  in 2000. He pursued graduate studies in Mo
 lecular Biology and Biomedicine at the University of Crete\, Greece\,  and
  Boston University\, USA. From 2007 to 2012\, he conducted postdoctoral re
 search at Columbia University\,  where he was later promoted to Associate 
 Research Scientist. In 2014\, he joined the Temple University School  of M
 edicine as a tenure-track Assistant Professor and was promoted to Associat
 e Professor with tenure in 2020.  In 2021\, he was appointed Ohio Eminent 
 Scholar and Professor of Pharmacology & Systems Physiology at the  Univers
 ity of Cincinnati College of Medicine.\nSpeakers:\nProfessor Konstantinos 
 Drosatos (University of Cincinnati College of Medicine)
LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3
 PT
TZID:Europe/London
URL:https://talks.ox.ac.uk/talks/id/e9c27fc9-05c0-4689-bf19-16f118fca48c/
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DESCRIPTION:Talk:FGF21 signaling activation: Treating obesity at the expen
 se of cardiac hypertrophy? - Professor Konstantinos Drosatos (University o
 f Cincinnati College of Medicine)
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