Skip to main content

Table 1 Adipokines in cardiac regulation

From: Cardiac-to-adipose axis in metabolic homeostasis and diseases: special instructions from the heart

Adipose location

Cellular type

Content/cargo

Healthy/pathological heart

Regulatory effects of cardiac function

Refs

Intrascapular BAT (iBAT)

Brown adipocyte

iNOS in sEV

Cardiac remodeling

Inducing the activation of cardiac fibroblasts (CFs)

Protecting against cardiac remodeling

[16]

Intrascapular BAT (iBAT)

Brown adipocyte

miR-125b-5p, miR-128-3p, miR-30d-5p in sEV

MI/R

Ameliorating MI/R-related cardiac dysfunction

Suppressing apoptosis by inhibition of MAPK pathway

[17]

Epididymal white adipose tissue (eWAT)

Adipocyte

miR-130b-3p in sEV

Diabetic MI/R

Increasing systolic/diastolic function

Decreasing infarct size in cardiac tissue

Promoting cardiomyocyte apoptosis

[18]

Pericardial adipose tissue

Adipocyte

Adipsin in sEV

MI

Alleviating MI-induced cardiac injury, including reduced myocardial fibrotic area and increased survival rate

Mitigating iron over-loading and lipid oxidative stress

[19]

Epicardial fat (eFat)

Not mentioned

Cytokines, miRNAs in sEV

AF

Stimulating cardiac fibrosis

Simulating angiogenesis by targeting endothelial cells

Promoting the initiation and maintenance of reentrant arrhythmias

[20]

Not mentioned

Macrophage

miR-140-5p in sEV

Obesity-induced cardiac injury

Provoking obvious cardiac injury

Inducing lipid peroxides and mitochondrial injury

Promoting ferroptosis in cardiomyocytes

[21]

In vitro

3T3-L1 adipocyte

miR-802-5p in sEV

Neonatal rat ventricular myocytes

Inducing insulin resistance and mitigating the insulin-sensitizing effects of adiponectin

Enhancing oxidative stress

[22]

In vitro

ADSC

SIRT1 in sEV

AMI

Increasing the survival rate

Reducing infarct size and post-AMI left ventricular remodeling;

Inducing vasculogenesis

Decreasing AMI-induced myocardial inflammation;

Promoting migration and tube formation of AMI-EPCs

[23]

In vitro

ADSC

miR-205 in sEV

AMI

Improving LVEF by alleviating MI-induced cardiac fibrosis

Reducing cardiomyocyte apoptosis

Increasing angiogenesis

[24]

In vitro

ADSC

miR-196a-5p, miR-425-5p in sEV

AMI

Preventing mitochondrial dysfunction and reactive oxygen species production

Increasing angiogenesis

Modulating macrophage polarization toward M2

Reducing myofibroblast activation and decreasing collagen expression

[25]

In vitro

ADSC

miR-320d in sEV

AF

Reducing apoptosis and increasing cell viability in cardiomyocytes

Activating STAT3 signaling pathway

[26]

Adipose tissue

Adipocyte

APN

MI

Improving cardiac function

[15]

Enhancing myocardial oxygen metabolism

[27]

Decreasing LSG function and neural activity

[40]

Suppressing ventricular arrhythmia

[41]

Adipose tissue

Adipocyte

omentin1

MI-induced HF

Ameliorating cardiac function, cardiac hypertrophy, infarct size and cardiac pathological features

[28]

Increasing mitochondrial fusion and decreasing mitochondrial fission

Promoting PINK1/Parkin-dependent mitophagy

Enhancing SIRT3/FOXO3a signaling

[42]

Adipose tissue

Adipocyte

FABP4

Obese heart

Depressing shortening amplitude in cardiomyocytes

Decreasing intracellular systolic peak Ca(2 +) in cardiomyocytes

Reducing the excitation–contraction gain

[29, 43]

Adipose tissue

Adipocyte

Resistin

MI/R

Improving left ventricular ejection fraction

Mitigating I/R-induced fibrosis;

Reducing atrial natriuretic peptide/brain natriuretic peptide expression

Inhibiting cardiomyocyte apoptosis

Promoting ADSC proliferation

[30, 31, 44]

Adipose tissue

Adipocyte

Apelin

Pressure overload-heart

Preventing myocardial fibrosis and cardiac remodelling

Inhibiting TGF-β1-mediated fibrotic response

[32, 45]

Adipose tissue

Adipocyte

CTRP3

Hypertension-induced cardiac hypertrophy

Restoring left ventricular cardiac contractile function

Alleviating cardiac hypertrophy and fibrosis;

Inhibiting expressions of hypertrophic and fibrotic signaling

Modulating endoplasmic reticulum stress

[33, 34, 46]

Visceral adipose tissue

Adipocyte

TNF-α, visfatin, HMGB1

Obese cardiac cells (in vitro)

Provoking apoptosis

Blocking differentiation

[35]

Visceral fat cell

Adipocyte

Vaspin

Sepsis-induced cardiac injury

Reducing mortality

Alleviating cardiac injury and cardiac dysfunction

Attenuating cardiac inflammation

Reducing cardiomyocyte apoptosis

[36, 47]

Pericardial adipose tissue

Adipocyte

Leptin

HFD- induced obesity

Exacerbating myocardial remodeling and dysfunction

Elevating oxidative stress and mitochondrial dysfunction in hearts

Stimulating apoptosis of cardiomyoblasts

[37, 48]

Epididymal and pericardial adipose tissue

White adipocyte

SFRP5

MI/R

Restoring cardiac function

Decreasing infarct size;

Inhibiting cardiac myocyte apoptosis and inflammation

[38, 49]

Brown adipose tissue

Brown adipocyte

Neuregulin-4

Diabetic cardiomyopathy

Alleviating myocardial injury

Upregulating autophagy via AMPK/mTOR pathway

[39]

  1. ADSCs adipose-derived stem cells; AF Atrial fibrillation; AMI acute myocardial infarction; APN Adiponectin; CTRP3 C1q-tumor necrosis factor-related protein-3; BAT brown adipose tissue; EPCs endothelial progenitor cells; FABP4 fatty acid-binding protein; HFD high-fat diet; iNOS inducible nitric oxide synthase; LSG: left stellate ganglion; LVEF left ventricular ejection fraction; MI myocardial infarction; MI-induced HF myocardial ischemia-induced heart failure; MI/R myocardial ischemia/reperfusion; MAPK mitogen-associated protein kinase; sEV small extracellular vesicle; SFRP5 secreted frizzled-related protein 5; SIRT1 Sirtuin 1; TGF-β1 transforming growth factor-β1