Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Vitamin K2 (MK7) alleviates arsenic-induced cardiac hypertrophy by suppressing the EGR3/BOK mitochondrial apoptosis pathway.
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Liu Ning, Zhao Qing, Xu Guowei, Li Bing
Аннотация
BACKGROUND: When arsenic combines with oxygen, chlorine and sulfur, it forms inorganic arsenic compounds. Studies have found that exposure to inorganic arsenic can cause pathological cardiac hypertrophy. MK7 is a long-chain menaquinone with superior bioavailability and extended half-life compared to other vitamin K2 homologues. BCL2-related ovarian killer (BOK) belongs to the BCL2 family and regulates mitochondrial membrane permeability to determine whether to initiate apoptosis. Early growth response 3 (EGR3) is a type of transcription factor that can specifically recognize and bind to its downstream regulatory gene promoter region, thereby exerting transcriptional regulation.
STUDY DESIGN: We investigated the underlying mechanism of MK7 as a prophylactic treatment for inorganic arsenic-induced pathological cardiac hypertrophy.
RESULTS: Inorganic arsenic exposure caused pathological cardiac hypertrophy in mice. MK7 inhibited the increase of the surface area of mouse cardiomyocytes, apoptosis, the expression of ANP and BNP, and the abnormalities of myocardial enzyme spectrum and cardiac function caused by inorganic arsenic, which were reversed by BOK and EGR3 overexpression. CHIP and dual luciferase reporting system results demonstrated that BOK was the direct target gene of EGR3.
CONCLUSION: MK7 alleviates inorganic arsenic-induced pathological cardiac hypertrophy by downregulating the EGR3-mediated transcriptional activation of BOK, thereby inhibiting the mitochondrial apoptosis pathway in cardiomyocytes.
STUDY DESIGN: We investigated the underlying mechanism of MK7 as a prophylactic treatment for inorganic arsenic-induced pathological cardiac hypertrophy.
RESULTS: Inorganic arsenic exposure caused pathological cardiac hypertrophy in mice. MK7 inhibited the increase of the surface area of mouse cardiomyocytes, apoptosis, the expression of ANP and BNP, and the abnormalities of myocardial enzyme spectrum and cardiac function caused by inorganic arsenic, which were reversed by BOK and EGR3 overexpression. CHIP and dual luciferase reporting system results demonstrated that BOK was the direct target gene of EGR3.
CONCLUSION: MK7 alleviates inorganic arsenic-induced pathological cardiac hypertrophy by downregulating the EGR3-mediated transcriptional activation of BOK, thereby inhibiting the mitochondrial apoptosis pathway in cardiomyocytes.