Postprandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons. Journal Article uri icon

Overview

abstract

  • Constricting pythons, known for their ability to consume infrequent, massive meals, exhibit rapid and reversible cardiac hypertrophy following feeding. Our primary goal was to investigate how python hearts achieve this adaptive response after feeding. Isolated myofibrils increased force after feeding without changes in sarcomere ultrastructure and without increasing energy cost. Ca2+ transients were prolonged after feeding with no changes in myofibril Ca2+ sensitivity. Feeding reduced titin-based tension, resulting in decreased cardiac tissue stiffness. Feeding also reduced the activity of sirtuins, a metabolically linked class of histone deacetylases, and increased chromatin accessibility. Transcription factor enrichment analysis on transposase-accessible chromatin with sequencing revealed the prominent role of transcription factors Yin Yang1 and NRF1 in postfeeding cardiac adaptation. Gene expression also changed with the enrichment of translation and metabolism. Finally, metabolomics analysis and adenosine triphosphate production demonstrated that cardiac adaptation after feeding not only increased energy demand but also energy production. These findings have broad implications for our understanding of cardiac adaptation across species and hold promise for the development of innovative approaches to address cardiovascular diseases.

publication date

  • September 3, 2024

has subject area

has restriction

  • hybrid

Date in CU Experts

  • August 22, 2024 2:20 AM

Full Author List

  • Crocini C; Woulfe KC; Ozeroff CD; Perni S; Cardiello J; Walker CJ; Wilson CE; Anseth K; Allen MA; Leinwand LA

author count

  • 10

Other Profiles

Electronic International Standard Serial Number (EISSN)

  • 1091-6490

Additional Document Info

start page

  • e2322726121

volume

  • 121

issue

  • 36