Asset Details
Do you wish to reserve the book?
Environment‐induced heat stress causes ventricular‐dependent biochemical changes in the heart in female pigs
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Environment‐induced heat stress causes ventricular‐dependent biochemical changes in the heart in female pigs
Do you wish to request the book?
Environment‐induced heat stress causes ventricular‐dependent biochemical changes in the heart in female pigs
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Environment‐induced heat stress causes ventricular‐dependent biochemical changes in the heart in female pigs
2025
Overview
Prolonged exposure to inescapable heat and humidity can lead to environment‐induced heat stress (EIHS). The extent to which EIHS damages the heart is largely unknown, though our previous work indicated EIHS caused ventricle‐dependent changes. The purpose of this investigation was to determine the extent to which EIHS increased proteolysis and altered calcium homeostasis in the left (LV) and right ventricles (RV). We hypothesized that in the RV, EIHS would increase proteolysis, whereas in the LV, EIHS would cause calcium dysregulation. To test this hypothesis, 3‐month‐old female pigs were assigned to thermoneutral (TN; 20 ± 0.2°C; n = 8) or EIHS (37.4 ± 0.2°C; n = 8) conditions for 24 h and hearts were removed. In the RV, we discovered increased markers of proteolysis such that the relative protein abundance of calpain II, MuRF‐1, and MAFbx/Atrogin1 was increased, as was a marker of calpain activity. Conversely, in the LV, we discovered that EIHS increased the relative protein abundance of calcium regulatory proteins, including PMCA, SERCA2a, STIM1, calsequestrin, CaMKII, and VDAC. These data demonstrate EIHS caused ventricular‐dependent changes such that in the RV, the balance of proteostasis was shifted toward proteolysis and in the LV, calcium dysregulation may underlie, at least in part, our previous discovery of ventricular thickening.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc,Wiley
