Besides its role as an energy storage organ, adipose tissue can be viewed as a dynamic and complex endocrine organ, which produces and secretes several adipokines, including hormones, cytokines, extracellular matrix (ECM) proteins, and growth and vasoactive factors. A wide body of evidence showed that adipokines play a critical role in various biological and physiological functions, among which feeding modulation, inflammatory and immune function, glucose and lipid metabolism, and blood pressure control. The aim of this review is to summarize the effects of several adipokines, including leptin, diponectin, resistin, chemerin, lipocalin-2 (LCN2), vaspin, omentin, follistatin-like 1 (FSTL1), secreted protein acidic and rich in cysteine (SPARC), secreted frizzled-related protein 5 (SFRP5), C1q/TNF-related proteins (CTRPs), family with sequence similarity to 19 member A5 (FAM19A5), wingless-type inducible signaling pathway protein-1 (WISP1), progranulin (PGRN), nesfatin-1 (nesfatin), visfatin/PBEF/NAMPT, apelin, retinol binding protein 4 (RPB4), and plasminogen activator inhibitor-1 (PAI-1) in the regulation of insulin resistance and vascular function, as well as many aspects of inflammation and immunity and their potential role in managing obesity-associated diseases, including metabolic, osteoarticular, and cardiovascular diseases.

/pdf/adipokines-new-potential-therapeutic-target-for-obesity-and-56yz3k8h2s.pdf

Adipokines: New Potential Therapeutic Target for Obesity and Metabolic, Rheumatic, and Cardiovascular Diseases.

Abnormal gene expression and secreted protein levels are accompanied by extensive pathological changes. Secreted frizzled related protein (SFRP) family members are antagonistic inhibitors of the Wnt signaling pathway, and they were recently found to be involved in the pathogenesis of a variety of metabolic diseases, which has led to extensive interest in SFRPs. Previous reports highlighted the importance of SFRPs in lipid metabolism, obesity, type 2 diabetes mellitus and cardiovascular diseases. In this review, we provide a detailed introduction of SFRPs, including their structural characteristics, receptors, inhibitors, signaling pathways and metabolic disease impacts. In addition to summarizing the pathologies and potential molecular mechanisms associated with SFRPs, this review further suggests the potential future use of SFRPs as disease biomarkers therapeutic targets.

/pdf/secreted-frizzled-related-proteins-in-cardiovascular-and-3il3raq65f.pdf

Secreted Frizzled Related Proteins in Cardiovascular and Metabolic Diseases.

Abstract Re-activating quiescent adult epicardium represents a potential therapeutic approach for human cardiac regeneration. However, the exact molecular differences between inactive adult and active fetal epicardium are not known. In this study, we combined fetal and adult human hearts using single-cell and single-nuclei RNA sequencing and compared epicardial cells from both stages. We found that a migratory fibroblast-like epicardial population only in the fetal heart and fetal epicardium expressed angiogenic gene programs, whereas the adult epicardium was solely mesothelial and immune responsive. Furthermore, we predicted that adult hearts may still receive fetal epicardial paracrine communication, including WNT signaling with endocardium, reinforcing the validity of regenerative strategies that administer or reactivate epicardial cells in situ. Finally, we explained graft efficacy of our human embryonic stem-cell-derived epicardium model by noting its similarity to human fetal epicardium. Overall, our study defines epicardial programs of regenerative angiogenesis absent in adult hearts, contextualizes animal studies and defines epicardial states required for effective human heart regeneration. 

/pdf/a-single-cell-comparison-of-adult-and-fetal-human-epicardium-3nh15h82.pdf

A single-cell comparison of adult and fetal human epicardium defines the age-associated changes in epicardial activity

According to the latest Global Burden of Disease Study, cardiovascular disease (CVD) is the leading cause of death, and ischemic heart disease and stroke are the cause of death in approximately half of CVD patients. In CVD, mitochondrial dysfunction following ischemia-reperfusion (I/R) injury results in heart failure. The proper functioning of oxidative phosphorylation (OXPHOS) and the mitochondrial life cycle in cardiac mitochondria are closely related to mitochondrial DNA (mtDNA). Following myocardial I/R injury, mitochondria activate multiple repair and clearance mechanisms to repair damaged mtDNA. When these repair mechanisms are insufficient to restore the structure and function of mtDNA, irreversible mtDNA damage occurs, leading to mtDNA mutations. Since mtDNA mutations aggravate OXPHOS dysfunction and affect mitophagy, mtDNA mutation accumulation leads to leakage of mtDNA and proteins outside the mitochondria, inducing an innate immune response, aggravating cardiovascular injury, and leading to the need for external interventions to stop or slow the disease course. On the other hand, mtDNA released into the circulation after cardiac injury can serve as a biomarker for CVD diagnosis and prognosis. This article reviews the pathogenic basis and related research findings of mtDNA oxidative damage and mtDNA leak-triggered innate immune response associated with I/R injury in CVD and summarizes therapeutic options that target mtDNA.

/pdf/mitochondrial-dna-is-a-vital-driving-force-in-ischemia-3e644yk3.pdf

Mitochondrial DNA Is a Vital Driving Force in Ischemia-Reperfusion Injury in Cardiovascular Diseases

Background: The association between abnormal invasive fractional flow reserve (FFR) and the fat attenuation index (FAI) of lesion-specific peri-coronary adipose tissue (PCAT) is unclear. Method: Data of patients who underwent coronary computed tomography angiography (CTA) and subsequent invasive coronary angiography (ICA) and FFR measurement within 1 week were retrospectively included. Lesion-specific FAI (FAIlesion), lesion-free FAI (FAInormal), epicardial adipose tissue (EAT) volume and attenuation was collected, along with stenosis severity and plaque characteristics. Lesions with FFR <0.8 were considered functionally significant. The association between FFR and each parameter was analyzed by logistic regression or receiver operating characteristic curve. Result: A total of 227 patients from seven centers were included. EAT volume or attenuation, traditional risk factors, and FAInormal (with vs. without ischemia: -82 ± 11 HU vs. -81 ± 11 HU, p = 0.65) were not significantly different in patients with or without abnormal FFR. In contrast, lesions causing functional ischemia presented more severe stenosis, greater plaque volume, and higher FAIlesion (with vs. without ischemia: -71 ± 8 HU vs. -76 ± 9 HU, p < 0.01). Additionally, the CTA-assessed stenosis severity (OR 1.06, 95%CI 1.04-1.08, p < 0.01) and FAIlesion (OR 1.08, 95%CI 1.04-1.12, p < 0.01) were determined to be independent factors that could predict ischemia. The combination model of these two CTA parameters exhibited a diagnostic value similar to the invasive coronary angiography (ICA)-assessed stenosis severity (AUC: 0.820 vs. 0.839, p = 0.39). Conclusion: It was FAIlesion, not general EAT parameters, that was independently associated with abnormal FFR and the diagnostic performance of CTA-assessed stenosis severity for functional ischemia was significantly improved in combination with FAIlesion.

Lesion-Specific Peri-Coronary Fat Attenuation Index Is Associated With Functional Myocardial Ischemia Defined by Abnormal Fractional Flow Reserve.

Aim: Several members of secreted frizzled-related protein (SFRP) are involved in the process of myocardial ischemia-reperfusion injury. However, little is known about the role of SFRP5 in patients with acute ST-segment elevation myocardial infarction (STEMI).

Methods: In this cross-sectional study, 85 patients with first-time anterior STEMI who underwent timely primary percutaneous coronary intervention (PCI) and 35 patients without coronary artery disease (CAD) were enrolled. Serum SFRP5 levels were measured using an enzyme-linked immunosorbent assay kit. Patients with STEMI were divided into low-SFRP5 and high-SFRP5 groups according to their median baseline serum SFRP5 levels. To evaluate cardiac function and structure after infarction, the left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume (LVEDV) were measured using echocardiography. The associations between changes in LVEF and reduced LVEF (≤ 50%) and clinical variables were determined by univariate and multivariate analyses.

Results: Baseline serum SFRP5 levels were significantly higher in patients with STEMI than in those without CAD (23.3 ng/mL vs 19.8 ng/mL, P = 0.008), although they decreased over time. Also, baseline serum SFRP5 levels were inversely correlated with peak hypersensitive cardiac troponin I (hs-cTnI) levels (r = −0.234, P = 0.025) and peak hypersensitive C-reactive protein (hs-CRP) levels (r = −0.262, P = 0.015). A multivariate linear regression model showed that changes in LVEF were positively correlated with serum SFRP5 levels at baseline (β = 0.249, 95% confidence interval (CI) 0.018–0.245, P = 0.024) and 24 h after admission (β = 0.220, 95% CI 0.003–0.264, P = 0.045). At 3 months, LVEF in patients with high SFRP5 levels was significantly improved over baseline [(60.8 ± 7.1) % vs (56.1 ± 7.5) %, P = 0.001]. LVEF was also significantly higher in patients with high SFRP5 levels than in those with low at the 3-month follow-up [(60.8 ± 7.1) % vs (56.8 ± 8.9) %, P = 0.028]. Consequently, high serum SFRP5 levels at baseline were associated with a decreased risk of reduced LVEF at 3 months, independent of peak hs-cTnI and baseline cardiac function (hazard ratio 0.190, 95% CI 0.036–0.996; P = 0.049).

Conclusions: High serum SFRP5 levels measured during the acute phase of STEMI were significantly associated with promoting myocardial recovery at an early phase following primary PCI, suggesting that SFRP5 is a potential therapeutic target in acute STEMI.

High Serum Secreted Frizzled-Related Protein 5 Levels Associates with Early Improvement of Cardiac Function Following ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention.

We aimed to investigate the association of lesion-specific epicardial adipose tissue (EAT) volume and density with the presence of myocardial ischemia. We enrolled 45 patients (55 lesions) with known or suspected coronary artery disease who underwent coronary computed tomography angiography (CTA) followed by invasive fractional flow reserve (FFR) assessment within 30 days. EAT volume (index) and density in patient-, vessel- and lesion-level were measured on CTA images. Lesion-specific ischemia was defined as a lesion with stenosis diameter > 90% or FFR ≤0.80. Multivariate analysis determined the independent association of EAT parameters with lesion-specific ischemia. Mean age of the patients was 60 years, and 75% were male. Overall, 55.6% of patients had ischemic lesions and a mean FFR baseline value of 0.82 ± 0.10. Total EAT volume index was significantly higher in patients with functionally or anatomically significant stenosis. Specifically, peri-lesion EAT volume index, not the density, was positively correlated with lesion-specific ischemia independent of luminal stenosis and plaque characteristics (hazard ratio 1.56, 95% confidence interval 1.04–2.33, P = 0.032; per 0.1 ml/m2 increase). Moreover, peri-lesion EAT volume was negatively correlated with lesion FFR values, whereas total EAT volume was positively correlated with fat accumulation and glucose metabolism. In addition, there was no association of EAT volume or density with myocardial ischemia in vessel-level analysis. Lesion-specific EAT volume index, but not density, seems positively and independently associated with myocardial ischemia, while its incremental diagnostic value of lesion-specific ischemia should be further investigated.

/pdf/relation-between-quantity-and-quality-of-peri-coronary-3zdvt06j1y.pdf

Relation between quantity and quality of peri-coronary epicardial adipose tissue and its underlying hemodynamically significant coronary stenosis.

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High Serum Secreted Frizzled-Related Protein 5 Levels Associates with Early Improvement of Cardiac Function Following ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention.

Relation between quantity and quality of peri-coronary epicardial adipose tissue and its underlying hemodynamically significant coronary stenosis.