TRPC5 Promotes Intermittent Hypoxia-Induced Cardiomyocyte Injury Through Oxidative Stress.
Level 4 - case-series / case-control
Case-control human study combined with in vitro mechanistic cell culture experiments
PubMed 39720578 · doi:10.2147/NSS.S494748
What was done
Evaluated peripheral blood TRPC5 mRNA expression and echocardiographic parameters in 30 newly diagnosed obstructive sleep apnea (OSA) patients and 30 primary snoring controls. In vitro, rat cardiomyoblast cells (H9c2) under intermittent hypoxia (IH) or normoxia were tested with or without TRPC5 overexpression and reactive oxygen species (ROS) inhibition via N-acetylcysteine (NAC) to measure cell viability, apoptosis, Ca2+ concentrations, ROS generation, and mitochondrial structure and membrane function.
What was found
OSA patients had significantly higher TRPC5 mRNA levels and left atrial diameter, and a lower E/A ratio compared to controls (all P < 0.05; exact numerical values not reported in abstract). In H9c2 cells, IH decreased viability, induced apoptosis, and increased TRPC5 expression (all P < 0.05). TRPC5 overexpression accelerated IH-induced oxidative stress, apoptosis, and mitochondrial structural and functional damage (all P < 0.05), effects that were attenuated by ROS inhibition with NAC.
Why it matters
Highlights TRPC5 and associated oxidative stress pathways as potential mechanistic mediators and therapeutic targets for myocardial injury in obstructive sleep apnea.
Limits
The human cohort was small (n = 60) and observational, preventing causal inference in clinical settings. Numerical baseline values, effect sizes, and confidence intervals were omitted from the abstract. Mechanistic findings rely on an immortalized rat cardiomyoblast cell line rather than primary human cardiomyocytes or intact in vivo models.