ArticleScientific reports2026
Huoxue Qianyang Qutan Recipe limits cardiac remodeling by regulating FUNDC1/IP3R2 signaling pathway in obese hypertensive rats.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Obese hypertension (OBH) increases cardiovascular risk through myocardial remodeling, which is associated with disrupted mitochondrial Ca²⁺ homeostasis and dysfunction of mitochondria-associated endoplasmic reticulum membranes (MAM). Huoxue Qianyang Qutan Recipe (HQQR) has been shown to lower blood pressure in OBH, but its mechanism related to MAM remains unclear. In this study, phenotypic assessments in OBH rats included blood pressure, morphological parameters, and cardiac ultrasound. Cardiomyocyte hypertrophy and mitochondrial Ca²⁺ levels were analyzed via pathological staining (assessed using fluorescence-based staining), while MAM ultrastructure was examined by electron microscopy. Additionally, the activity of mitochondrial respiratory chain Complexes I-IV was detected in vivo to evaluate mitochondrial respiratory function. In vitro, flow cytometry was used to evaluate mitochondrial Ca²⁺, mitochondrial reactive oxygen species (mitoROS), and membrane potential. Protein levels of FUNDC1 and IP3R2 were assessed. Co-immunoprecipitation revealed an interaction between FUNDC1 and IP3R2, and further experiments with FUNDC1 siRNA knockdown and overexpression were conducted to clarify the mechanism of HQQR. Results showed that HQQR significantly lowered blood pressure, reduced left ventricular mass, and alleviated cardiomyocyte hypertrophy in OBH rats. In vivo, HQQR altered MAM structure and function, facilitated mitochondrial Ca²⁺ transport, and modulated FUNDC1 and IP3R2 expression. In vitro, HQQR reduced mitoROS and preserved mitochondrial Ca²⁺ homeostasis. Both HQQR treatment and FUNDC1 knockdown attenuated angiotensin II-induced cardiomyocyte hypertrophy and mitochondrial damage, as indicated by decreased levels of ANP, BNP, β-MHC, mitochondrial Ca²⁺, and mitoROS. In contrast, FUNDC1 overexpression diminished the protective effects of HQQR. The interaction between FUNDC1 and IP3R2 was confirmed, and the decrease in IP3R2 may be associated with ubiquitination-mediated degradation. In conclusion, HQQR mitigates MAM dysfunction in OBH-induced myocardial remodeling by regulating the FUNDC1-IP3R2 interaction and promoting ubiquitin-dependent degradation of IP3R2, thereby maintaining mitochondrial Ca²⁺ homeostasis in cardiomyocytes.
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