The abstract is read at the publisher; the summary is JClub's.
CD36 deficiency in mice disrupts circadian blood pressure rhythms, producing significantly higher daytime BP, and platelet CD36 levels are linked to nocturnal hypertension severity in humans.
- Why it matters: Nocturnal hypertension strongly predicts cardio-cerebrovascular disease, but the mechanisms controlling blood pressure rhythms are unclear, limiting targeted prediction and therapy.
- What they did: The study used 48-hour telemetry in CD36 global knockout and renal proximal tubule-specific CD36 knockout mice, plus human ambulatory BP data and serum measures to relate CD36 expression to nocturnal hypertension; it also screened factors to define the AMPK/HDAC5/PER1 mechanism.
- The result: CD36 modulates BP rhythms via AMPK/HDAC5/PER1: deficiency activates phosphorylated AMPK, disrupts the HDAC5-PER1 complex, increases PER1 nuclear accumulation, and desynchronizes intrarenal gene oscillations, implying CD36 as a potential predictor and therapeutic target.
The findingWhy it mattersWhat they didThe result
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