Adipocyte-derived chemerin rescues lipid overload-induced cardiac dysfunction

Liu, Ruimin; Han, Yinying; Huang, Cheng‐Long; Hou, Mengqian; Chen, Rui; Wang, Shujin; Li, Xi; Tian, Jie

doi:10.1016/j.isci.2023.106495

Cited by 2 publications

(1 citation statement)

References 45 publications

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“…Given the existence of multiple isoforms in the case of both chemerin and PlGF, 8,10,[32][33][34][35][36] we used human retinoic acid receptor responder 2 small interfering RNA (small interfering-Chemerin, 10 nmol/L; Thermo Fisher Scientific, 12179), and human PlGF siRNA (small interfering-PlGF, 50 nmol/L; Thermo Fisher Scientific, 143789) to knockdown chemerin and PlGF in HepG2 cells (ATCC, Manassas, VA) and placenta villous explants. 37,38 A nontargeting siRNA (small interfering control) was used as a negative control (Thermo Fisher Scientific, AM4611).…”

Section: Western Blottingmentioning

confidence: 99%

Statins Prevent the Deleterious Consequences of Placental Chemerin Upregulation in Preeclampsia

Tan,

Kluivers,

Cruz-López

et al. 2024

Hypertension

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BACKGROUND: Chemerin, an inflammatory adipokine, is upregulated in preeclampsia, and its placental overexpression results in preeclampsia-like symptoms in mice. Statins may lower chemerin. METHODS: Chemerin was determined in a prospective cohort study in women suspected of preeclampsia and evaluated as a predictor versus the sFlt-1 (soluble fms-like tyrosine kinase-1)/PlGF (placental growth factor) ratio. Chemerin release was studied in perfused placentas and placental explants with or without the statins pravastatin and fluvastatin. We also addressed statin placental passage and the effects of chemerin in chorionic plate arteries. RESULTS: Serum chemerin was elevated in women with preeclampsia, and its addition to a predictive model yielded significant effects on top of the sFlt-1/PlGF ratio to predict preeclampsia and its fetal complications. Perfused placentas and explants of preeclamptic women released more chemerin and sFlt-1 and less PlGF than those of healthy pregnant women. Statins reversed this. Both statins entered the fetal compartment, and the fetal/maternal concentration ratio of pravastatin was twice that of fluvastatin. Chemerin constricted plate arteries, and this was blocked by a chemerin receptor antagonist and pravastatin. Chemerin did not potentiate endothelin-1 in chorionic plate arteries. In explants, statins upregulated low-density lipoprotein receptor expression, which relies on the same transcription factor as chemerin, and NO release. CONCLUSIONS: Chemerin is a biomarker for preeclampsia, and statins both prevent its placental upregulation and effects, in an NO and low-density lipoprotein receptor–dependent manner. Combined with their capacity to improve the sFlt-1/PlGF ratio, this offers an attractive mechanism by which statins may prevent or treat preeclampsia.

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Section: Western Blottingmentioning

confidence: 99%

Statins Prevent the Deleterious Consequences of Placental Chemerin Upregulation in Preeclampsia

Tan,

Kluivers,

Cruz-López

et al. 2024

Hypertension

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Chemerin in the Spotlight: Revealing Its Multifaceted Role in Acute Myocardial Infarction

Mitsis,

Khattab,

Myrianthefs

et al. 2024

Biomedicines

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Chemerin, an adipokine known for its role in adipogenesis and inflammation, has emerged as a significant biomarker in cardiovascular diseases, including acute myocardial infarction (AMI). Recent studies have highlighted chemerin’s involvement in the pathophysiological processes of coronary artery disease (CAD), where it modulates inflammatory responses, endothelial function, and vascular remodelling. Elevated levels of chemerin have been associated with adverse cardiovascular outcomes, including increased myocardial injury, left ventricular dysfunction, and heightened inflammatory states post-AMI. This manuscript aims to provide a comprehensive review of the current understanding of chemerin’s role in AMI, detailing its molecular mechanisms, clinical implications, and potential as a biomarker for diagnosis and prognosis. Additionally, we explore the therapeutic prospects of targeting chemerin pathways to mitigate myocardial damage and improve clinical outcomes in AMI patients. By synthesizing the latest research findings, this review seeks to elucidate the multifaceted role of chemerin in AMI and its promise as a target for innovative therapeutic strategies.

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Adipocyte-derived chemerin rescues lipid overload-induced cardiac dysfunction

Cited by 2 publications

References 45 publications

Statins Prevent the Deleterious Consequences of Placental Chemerin Upregulation in Preeclampsia

Statins Prevent the Deleterious Consequences of Placental Chemerin Upregulation in Preeclampsia

Chemerin in the Spotlight: Revealing Its Multifaceted Role in Acute Myocardial Infarction

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