Role of major adipokines in hypertension: A literature review

Table 1 Summary of studies which reported the major adipokine's role in hypertension patients

Ref.	Adipokines	The main finding in the pathogenesis of hypertension
David et al[5], 2020	Chemerin	The long-term remodeling of blood vessels in hypertension was the proliferative effect which might be influenced due to the chemerin
Gu et al[6], 2014	Chemerin	Chemerin is strongly associated with markers of inflammation and components of the metabolic syndrome in hypertensive subjects and was independently associated with hypertension after adjustment for age, gender and metabolic risk factors
Gu et al[7], 2015	Chemerin	Chemerin levels were independently associated with the index of arterial function and early atherosclerosis in essential hypertension
Wójcik et al[8], 2020	Chemerin	Elevated chemerin levels may be associated with increased systolic blood pressure in obese children
Yamamoto et al[9], 2021	Chemerin (CMKLR1)	For the first time revealed that the increased protein expression of CMKLR1 in the paraventricular nucleus was at least partly responsible for systemic hypertension in spontaneously hypertensive rats SHR
Ferland et al[10], 2019	Chemerin	Chemerin, not derived from the liver but potentially from adipose tissue, is an important driver of hypertension associated with high fat
Gunes et al[11], 2012	Visfatin	The mean visfatin level was significantly higher in hypertensive patients
Wang et al[12], 2010	Visfatin	Serum visfatin levels in Lyon hypertensive rats were elevated and associated with lipid metabolic abnormalities
Liakos et al[13], 2015	Visfatin, apelin	The lower apelin and higher visfatin plasma levels in high normal BP subjects compared to normal or optimal BP individuals could partially explain the higher CV risk of the high normal BP group
Yu et al[14], 2019	Visfatin	Association of hypertension and cerebrovascular accident with higher plasma visfatin levels
Kocelak et al[15], 2014	Visfatin/NAMPT	The presence of hypertension was not associated with the plasma levels of visfatin/NAMPT in elderly subjects
Hsu et al[16], 2016	Visfatin	Reported the association with subsequent renal function with increased circulating visfatin in nondiabetic hypertensive patients
Parimelazhagan et al[17], 2021	Visfatin	Found a positive correlation between visfatin and diastolic blood pressure as well as high-density lipoproteins
Rotkegel et al[18], 2013	Visfatin	Increased plasma visfatin concentration may play a significant role in the pathogenesis of hypertension in patients with visceral obesity
Kraus et al[20], 2015	RBP4	Elevated levels RBP4 contribute to insulin resistance and were correlated with increased prevalence of hypertension and myocardial infarction
Li et al[21], 2019	RBP4	RBP4 levels were closely correlated with blood pressure levels and might be involved in the regulation of left ventricular diastolic function in patients with essential hypertension
Deng et al[27], 2014	RBP4	RBP4 levels were increased in naive hypertensive patients; however, no differences were observed in obese or non-obese hypertensive subjects
Solini et al[22], 2009	RBP4	Retinol-binding protein-4 levels were increased in naïve hypertensive women and correlated with the degree of carotid intima-media thickness suggesting the participation of this adipocytokine in the modulation of the atherosclerotic process exert by the adipose tissue as an endocrine organ
Zhang et al[28], 2017	RBP4	Serum RBP4 level was significantly higher and closely associated with BP in prehypertensive Chinese
Stuck et al[29], 2010	RBP4	Lowering serum RBP4 may be a novel therapeutic tool for hypertension with additive effects to current standard treatments that focus on the inhibition of the angiotensin system
Peng et al[30], 2017	PAI-1	Plasma PAI-1 may contribute to the development of hypertension through pathways beyond traditional risk factors
Srikumar et al[31], 2002	PAI-1	PAI-1 levels were correlated with plasma renin activity, aldosterone, and insulin resistance in hypertensive subjects
Kaikita et al[32], 2001	PAI-1	Direct inhibition of vascular PAI-1 activity may provide a new therapeutic strategy for the prevention of arteriosclerotic cardiovascular disease
Ritter et al[34], 2017	MCP-1	The study suggests a possible downregulation in MCP-1 levels in hypertensive individuals with LVH, regardless of hypertension strata
Wang et al[35], 2015	MCP-1	Indicate that deletion of transient receptor potential vanilloid type 1 TRPV1 aggravated the renal injury in salt-sensitive hypertension via enhancing MCP-1/CCR2 signaling-dependent inflammatory responses
Çelik et al[36], 2021	Omentin-1	Authors demonstrated that serum omentin-1 levels decreased in patients with hypertension as compared with normotensive controls, which could be attributed to a combined outcome of endothelial dysfunction, inflammation as well as renal injury in the setting of hypertension
Dong et al[37], 2021	Omentin-1	The down-regulation of omentin-1 induces endothelial dysfunction and hypertension in obesity. Tetrahydroxystilbene glycoside treatment (at least partially) increases omentin-1 via promoting the binding of peroxisome proliferator-activated receptor-γ (PPAR-γ) and intelectin-1 (Itln-1) promoter in adipose tissues, subsequently exerts protective effects on endothelial function via activating Akt/eNOS/NO signaling and attenuating oxidative/nitrative stress
Cetin et al[38], 2022	Omentin-1	The study suggests that circulating omentin-1 levels were inversely related to the presence of MetS and may be a reliable marker to predict the development of MetS in patients with hypertension
Song et al[39], 2014	Lipocalin-2	Administration of lipocalin-2 causes abnormal vasodilator responses in mice on a high-fat diet. Polyamination facilitates the clearance of lipocalin-2, whereas the accumulation of deamidated lipocalin-2 in arteries causes vascular inflammation, endothelial dysfunction, and hypertension
Ong et al[40], 2011	LCN2	The author's findings suggest, for the first time, that genetic variants in LCN2 may affect BP
Chen et al[41], 2020	LCN2	The contributing role of LCN2 in liver fibrosis as well as portal hypertension in alcoholic hepatitis and might represent a new therapeutic target
Kameshima et al[42], 2015	Vaspin	A study for the first time demonstrates that vaspin prevents the increase of SBP in SHR by inhibiting peripheral vascular hypertrophy, possibly via antioxidative and anti-inflammatory mechanisms
Fathey et al[43], 2022	Vaspin	Plasma vaspin may be used as an independent predictive biomarker for the early detection of macrovascular and/or microvascular hypertensive complications
Kaur et al[45], 2020	PGRN	Findings of reduced PGRN/TNF ratio, and it was an independent predictor of SBP, ascertain the key role of imbalance in the pro-and anti-inflammatory environment in hypertension
Han et al[47], 2018	CTRP1	CTRP1 contributes to the regulation of BP homeostasis by preventing dehydration-induced hypotension
Su et al[48], 2019	CTRP1	CTRP1 levels were increased and associated with STOD (heart and kidney) in essential hypertension, which can be regarded as a novel biomarker in the prediction of prognosis for patients with essential hypertension
Seccia et al[49], 2010	CTRP1	CTRP-1 was expressed in myelolipomas together with adenomas that produce aldosterone raising the possibility that CTRP-1 may cause an excess of aldosterone and the growth of ZG cells
Osaki et al[50], 2014	Nesfatin-1	Nesfatin-1 may probably be a new key molecule involved in hypertension and can be used as an anti-obesity and anti-T2DM medication
Zhao et al[51], 2015	Nesfatin-1	Fasting plasma nesfatin-1 levels were significantly higher in hypertension patients than in the control group, especially in overweight/obese hypertension patients
Güneş et al[52], 2020	Nesfatin-1	Nesfatin-1 levels were higher and an independent predictor of hypertension in obese subjects
Lu et al[53], 2018	Nesfatin-1	Nesfatin-1 is a key modulator in hypertension and vascular remodeling by facilitating vascular smooth muscle cells phenotypic switching and proliferation

CV: Cardiovascular; NAMPT: Nicotinamide phosphoribosyl transferase; RBP4: Retinol-binding protein 4; PAI-1: Plasminogen activator inhibitor-1; MCP-1: Monocyte chemotactic protein-1; LVH: Left ventricular hypertrophy; CCR2: C-C chemokine receptor type 2; BP: Blood pressure; LCN2: Lipocalin-2; SBP: Systolic blood pressure; SHR: Spontaneously hypertensive rats; PGRN: Progranulin; TNF: Tumor necrosis factor; CTRP1: C1q/TNF-α–related protein 1; STOD: Subclinical target organ damage; ZG: Zona glomerulosa.