ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.
R, C., Q, M., G, L., S, Y., C, L., X, Z., & D, Z. (2026). ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.. Clinical and experimental pharmacology & physiology. https://doi.org/10.1111/1440-1681.70153
R C, Q M, G L, S Y, C L, X Z, et al. ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.. Clinical and experimental pharmacology & physiology. 2026; doi: 10.1111/1440-1681.70153
R C, Q M, G L, et al. ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.[J]. Clinical and experimental pharmacology & physiology. 2026. DOI: 10.1111/1440-1681.70153.
@article{r2026,
author = {Cao R and Meng Q and Li G and Yuan S and Li C and Zhao X and Zhang D},
title = {ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy.},
journal = {Clinical and experimental pharmacology & physiology},
year = {2026},
doi = {10.1111/1440-1681.70153},
note = {PMID: 42669620},
}
TY - JOUR AU - Cao R AU - Meng Q AU - Li G AU - Yuan S AU - Li C AU - Zhao X AU - Zhang D TI - ANGII Initiated HSF2 Trans-Activating HIF-1α Through Induction of ER Stress to Promote Cardiac Hypertrophy. T2 - Clinical and experimental pharmacology & physiology PY - 2026 DO - 10.1111/1440-1681.70153 AN - PMID:42669620 ER -
Heat shock factor 2 (HSF2) and hypoxia-inducible factor 1α are activated by angiotensin II (ANGII) in cardiomyocytes. The endoplasmic reticulum (ER) stress plays a critical role in cardiac hypertrophy. Moreover, HIF-1α is known to be regulated by HSF2 in tumour cells. In this study, we hypothesised and clarified whether HSF2 trans-activated HIF-1α through initiation of ER stress in hypertrophic cardiomyocytes. Myocardial hypertrophy was induced by the treatment of ANGII. Expression of the gene or protein was assessed by applying RT-PCR, WB, ICC and IHC. Luciferase and CHIP were applied to detect the transcription of HIF-1α by HSF2. Both in vitro and in vivo, the expression of HIF-1α, ER stress markers and HSF2 was increased in ANGII-treated hypertrophic cardiomyocytes. Blocking ER stress suppressed the expression of HSF2 and HIF-1α in ANGII-treated cardiomyocytes. Silencing HSF2 inhibited HIF-1α, thereby reducing hypertrophy but had no effect on ER stress. Similarly, silencing HIF-1α reduced hypertrophy without affecting ER stress or HSF2 expression. HSF2 transcriptionally activated HIF-1α. We concluded that ER stress induced by ANGII activates HSF2, which then trans-activates HIF-1α, promoting cardiac hypertrophy.