Key result
Elevated CTRP9 levels were positively correlated with carotid atherosclerotic plaque in hypertensive patients, and recombinant CTRP9 reduced atherosclerotic area in mice.
Why the study?
CTRP9 is an important adipocytokine closely linked to cardiovascular disease, but its expression in hypertension and effects on hypertension-related atherogenesis required investigation.
Does CTRP9 expression correlate with hypertension and does recombinant CTRP9 alleviate hypertension-related atherogenesis?
Observational
Does CTRP9 expression correlate with hypertension and does recombinant CTRP9 alleviate hypertension-related atherogenesis?
CTRP9 is elevated in hypertension and its administration in preclinical models reduces hypertension-related atherosclerosis and endothelial dysfunction, suggesting a compensatory protective role.
C1q‐tumor necrosis factor‐related protein‐9 (CTRP9) is an important adipocytokine that is closely associated with cardiovascular disease. This study aimed to detect CTRP9 expression in hypertensive patients and mice and to analyze its effects on hypertension‐related atherogenesis. First, circulating CTRP9 levels were detected in both nonhypertensive subjects and hypertensive patients. The results showed that plasma CTRP9 levels were increased in hypertension patients compared with control subjects and gradually elevated in the Grade I, Grade II, and Grade III groups. While nondipper state did not affect CTRP9 expression in hypertension patients. Hypertension patients with carotid atherosclerotic plaque (CAP) exhibited higher CTRP9 levels and the high CTRP9 group exhibited significantly higher CAP morbidity, CTRP9 levels were positively correlated with the occurrence of CAP. Then, effects of CTRP9 on angiotensin II (Ang II)‐induced endothelial dysfunction were analyzed in vitro, and the results exhibited that treatment with Ang II significantly increased CTRP9 mRNA expression in endothelial cells (ECs), and downregulation of CTRP9 expression aggravated Ang II‐induced endothelial dysfunction in ECs. Mice were infused with Ang II, and CTRP9 was also increased in Ang II‐infused mice and mainly secreted by ECs. In Ang II‐infused ApoE−/− mice, treatment with recombinant CTRP9 significantly reduced atherosclerotic area and alleviated endothelial dysfunction. In conclusion, our results may found that CTRP9 delayed the progression of hypertension‐related arteriosclerosis by alleviating endothelial dysfunction.
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Zhou et al. (2020) conducted an observational in Hypertension and hypertension-related atherogenesis. CTRP9 levels vs. Nonhypertensive subjects was evaluated on CTRP9 expression and occurrence of carotid atherosclerotic plaque. Elevated CTRP9 levels were positively correlated with carotid atherosclerotic plaque in hypertensive patients, and recombinant CTRP9 reduced atherosclerotic area in mice.
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