Key result
Cardiac TrkB knockout in mice worsens heart failure and blunts exercise adaptation by decreasing cellular energetics.
Why the study?
BDNF is markedly decreased in heart failure patients, but the role of myocardial BDNF signalling in cardiac pathophysiology remains poorly understood.
Population
Mice exposed to exercise or TAC, and human failing hearts
Comparison
cTrkB KO mice vs controls under exercise or TAC
Design
Preclinical animal and human tissue mechanistic study
Authors
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TrkB signaling may support cardiac energetics under stress; leaves open therapeutic targeting in human HF.
Myocardial BDNF plays a critical role in regulating cellular energetics in the cardiac stress response through the Yin Yang 1/PGC-1α pathway.
Yang et al. (2022) studied Heart failure. Cardiac-specific TrkB knockout vs. Wild-type controls was evaluated on Cardiac adaptive response to exercise and pathological stress. Cardiac-specific TrkB knockout in mice exacerbated heart failure progression and blunted adaptive responses to exercise by decreasing cellular energetics via the Yin Yang 1/PGC-1α pathway.
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