Key result
Rho A/ROCK1 signaling is significantly upregulated in human calcified aortic valves and promotes valvular calcification by driving metabolic reprogramming of interstitial cells toward the Warburg effect.
Why the study?
How Rho A/ROCK1 signaling transduces mechanical signals into cellular responses and disrupts normal valvular interstitial cell homeostasis remains unclear.
Does ROCK1 inhibition prevent osteogenic differentiation and calcification in human valvular interstitial cells?
Observational (n=34)
No
Does ROCK1 inhibition prevent osteogenic differentiation and calcification in human valvular interstitial cells?
Rho A/ROCK1 signaling promotes aortic valve calcification by driving metabolic reprogramming of valvular interstitial cells toward the Warburg effect, suggesting a potential therapeutic target for CAVD.
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RhoA/ROCK1 signaling in human CAVD valves leaves open its mechanistic role in VIC osteogenic differentiation; prospective studies needed before targeting.
Liu et al. (2023) conducted an observational in Calcific aortic valve disease (CAVD) (n=34). Rho A/ROCK1 signaling vs. Normal controls was evaluated on Protein expression of Rho A/ROCK1 and markers of osteogenic differentiation and Warburg effect. Rho A/ROCK1 signaling is significantly upregulated in human calcified aortic valves and promotes valvular calcification by driving metabolic reprogramming of interstitial cells toward the Warburg effect.
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