Kielin/chordin-like protein deficiency aggravates pressure overload-induced cardiac dysfunction and remodeling via P53/P21/CCNB1 signaling in mice.

Targeting cardiac remodeling is regarded as a key therapeutic strategy for heart failure. Kielin/chordin-like protein (KCP) is a secretory protein with 18 cysteine-rich domains and associated with kidney and liver fibrosis. However, the relationship between KCP and cardiac remodeling remains unclear.

Circulating IL-37 levels are elevated in patients with hypertension.

Interleukin-37 (IL-37) has been reported to be closely linked to vascular diseases, including atherosclerosis and aortic calcification. The present study aimed to assess the expression levels of IL-37 in patients with hypertension. Blood samples were collected from control subjects (n=20) and patients with hypertension (n=45).

Effect of N-acetylcysteine on prevention of contrast-associated acute kidney injury in patients with STEMI undergoing primary percutaneous coronary intervention: a systematic review and meta-analysis of randomised controlled trials.

Objective: Several studies evaluating the preventive effect of N-acetylcysteine (NAC) on contrast-associated acute kidney injury (CA-AKI) among patients with ST segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI) have suggested inconsistent results and that a systematic review and meta-analysis should be performed.

Design: Systematic review and meta-analysis.

Data Sources: PubMed, MEDLINE, EMBASE, ClinicalTrials.

ADAMTS-5 Decreases in Aortas and Plasma From Aortic Dissection Patients and Alleviates Angiotensin II-Induced Smooth Muscle-Cell Apoptosis.

Acute aortic dissection (AAD) is associated with degeneration of the aortic media and accompanied by vascular extracellular matrix (ECM) remodeling. Recently, a disintegrin and metalloproteinase with thrombospondin type 1 motifs-5 (ADAMTS-5) has been reported to be involved in ECM remodeling and vascular diseases. The aim of this study was to examine ADAMTS-5 levels in AAD patients and investigate the underlying mechanisms.

Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice.

Several interleukin (IL) family members have been demonstrated to be involved in doxorubicin (DOX)-induced cardiac injury. This study aimed to investigate the role of IL-22 in DOX-induced cardiac injury and explore its possible mechanisms. In this study, mice were given DOX, and the cardiac expression and sources of IL-22 were determined.

IL-35 polymorphisms and cognitive decline did not show any association in patients with coronary heart disease over a 2-year period: A retrospective observational study (STROBE compliant).

Prior evidence suggested that inflammation and inflammatory cytokines polymorphisms might be essential in the development of coronary heart disease (CHD) and cognitive decline. The following study investigated the associations between interleukin-35 (IL-35) polymorphisms and cognitive decline in CHD patients over a 2-year period.CHD patients were enrolled between January 2015 and January 2016.

Interleukin-22 is elevated in the atrium and plasma of patients with atrial fibrillation and increases collagen synthesis in transforming growth factor-β1-treated cardiac fibroblasts via the JNK pathway.

Our previous studies demonstrated that interleukin (IL)-22 is involved in cardiovascular diseases such as hypertension, cardiac fibrosis and aortic dissection. The purpose of the present study was to detect IL-22 expression in patients with atrial fibrillation (AF). Atrial tissue was collected from donors with sinus rhythm and patients with permanent AF, and the expression level of IL-22 and its receptors (IL-22R1 and IL-10R2) in both the left atrium (LA) and right atrium (RA) of each sample was detected.

Circulating Sestrin Levels Are Increased in Hypertension Patients.

Background: Sestrins (Sesns), a group of oxidative stress-related proteins, have been reported to be involved in various cardiovascular diseases, including aortic dissection and chronic heart failure. This study is aimed at investigating the level of circulating Sesn1, Sesn2, and Sesn3 in hypertension patients.

Methods: Plasma levels of Sesn1, Sesn2, and Sesn3 in 400 hypertensive patients and 100 normotensive subjects were detected using enzyme-linked immunosorbent assay (ELISA) kits.

A single-center observational study on the expression of circulating interleukin-20 levels and predicting outcomes in human chronic heart failure: A 2-year follow-up cohort study: Higher IL-20 levels suggest poorer outcomes in CHF patients.

Background: Interleukin-20 (IL-20) is closely related to cardiovascular diseases such as atherosclerosis. The relevance of IL-20 expression in human chronic heart failure (CHF) remains unknown. Thus, we investigated the level of circulating IL-20 in CHF patients and observed its correlation with CHF outcomes.

The Expression of IL-12 Family Members in Patients with Hypertension and Its Association with the Occurrence of Carotid Atherosclerosis.

Background: The interleukin-12 (IL-12) family consists of four members, namely, IL-12, IL-23, IL-27, and IL-35. The aim of this study was to examine the expression of circulating IL-12, IL-23, IL-27, and IL-35 in hypertensive patients.

Methods: Blood samples were collected from hypertensive patients and nonhypertensive (control) subjects, and protein multifactorial monitor kits were used to measure the plasma IL-12, IL-23, IL-27, and IL-35 levels in each sample.

Roles and Mechanisms of Interleukin-12 Family Members in Cardiovascular Diseases: Opportunities and Challenges.

Cardiovascular diseases represent a complex group of clinical syndromes caused by a variety of interacting pathological factors. They include the most extensive disease population and rank first in all-cause mortality worldwide. Accumulating evidence demonstrates that cytokines play critical roles in the presence and development of cardiovascular diseases.

Anti-interleukin-5-neutralizing antibody attenuates caradiac injury and cadiac dysfunction by aggravating the inflammatory response in doxorubicin-treated mice.

Previous studies have demonstrated that interleukins (ILs) are closely associated with doxorubicin (DOX)-induced cardiac injury. IL-5 is an important member of the IL family, and this study was performed to investigate whether IL-5 affects DOX-induced cardiac injury and its underlying mechanisms. The cardiac IL-5 expression was first detected and the results showed that cardiac IL-5 levels were significantly lower in DOX-treated mice, and IL-5 was mainly derived from cardiac macrophage (Mø).

IL-22 produced by Th22 cells aggravates atherosclerosis development in ApoE mice by enhancing DC-induced Th17 cell proliferation.

Th22 cells are a novel subset of CD4 T cells that primarily mediate biological effects through IL-22, with both Th22 cells and IL-22 being closely associated with multiple autoimmune and chronic inflammatory diseases. In this study, we investigated whether and how Th22 cells affect atherosclerosis. ApoE mice and age-matched C57BL/6J mice were fed a Western diet for 0, 4, 8 or 12 weeks.

Interleukin-12p35 deficiency enhances mitochondrial dysfunction and aggravates cardiac remodeling in aging mice.

Our previous studies have demonstrated that interleukin-12p35 knockout (IL-12p35 KO) regulates the progression of various cardiovascular diseases, such as acute cardiac injury and hypertension. The aims of this study were to investigate whether IL-12p35 KO affects aging-related cardiac remodeling and to explore the possible mechanisms. First, the effects of IL-12p35 KO on heart structure and function were detected, and the results showed that IL-12p35 KO exacerbated cardiac remodeling and increased cardiac senescence-related protein levels in aged mice.

Effects of circulating levels of Th17 cells on the outcomes of acute Stanford B aortic dissection patients after thoracic endovascular aortic repair: A 36-month follow-up study a cohort study.

T helper 17 (Th17) cells are related to the progression of aortic dissection. This study aimed to determine whether circulating Th17 levels are associated with the prognosis of acute Stanford type B aortic dissection (STBAD) after thoracic endovascular aortic repair (TEVAR).A cohort study was performed and STBAD patients (n = 140) received TEVAR were enrolled, the circulating Th17 levels were measured and the patients were divided into low and high Th17 groups, and 36 months of follow-up was performed.

Interleukin-32 increases in coronary arteries and plasma from patients with coronary artery disease.

Background: Interleukin-32 (IL-32) is a cytokine associated with higher risk of cardiovascular diseases in inflammatory environments. This study aimed to investigate the IL-32 levels in coronary artery disease (CAD) patients.

Methods: IL-32 expression in coronary arteries from both normal donors and CAD patients were analyzed.

Type 2 diabetes mellitus reduces clinical complications and mortality in Stanford type B aortic dissection after thoracic endovascular aortic repair: A 3-year follow-up study.

Background: Previous studies have demonstrated that type 2 diabetes mellitus (T2DM) is negatively correlated with the occurrence of aortic dissection (AD). This study aimed to investigate the effects of T2DM on the prognosis of Stanford type B AD (STBAD) patients after thoracic endovascular aortic repair (TEVAR).

Methods: STBAD patients (n = 141) who underwent TEVAR received an oral glucose tolerance test (OGTT) and were divided into a normal glucose (NG, n = 55) group, an abnormal glucose tolerance (AGT, n = 48) group and a T2DM (n = 38) group according to the results of the OGTT.

IL-37 inhibits the maturation of dendritic cells through the IL-1R8-TLR4-NF-κB pathway.

Mature dendritic cells (DCs) play a pathogenic role in atherosclerosis. Our previous study demonstrated that exogenous interleukin (IL)-37 suppresses the maturation of DCs, induces the T-regulatory (Treg) cell response, and attenuates atherosclerosis in ApoE mice. The aim of the present study was to explore the molecular mechanism of IL-37 on the maturation of DCs throughout the development of atherosclerosis.

Interleukin-12p35 Deficiency Reverses the Th1/Th2 Imbalance, Aggravates the Th17/Treg Imbalance, and Ameliorates Atherosclerosis in ApoE-/- Mice.

Interleukin- (IL-) 35, a novel functional cytokine of regulatory T cells (Treg) comprised of the IL-12p35 subunit and the other subunit Epstein-Barr virus-induced gene 3 (EBI3), regulates the activity of CD4+ T cells and macrophages, thereby playing a critical role in inflammatory and autoimmune diseases. Previous studies demonstrated that both recombinant mice and human IL-35 attenuated atherosclerosis in ApoE-/- mice. Additionally, EBI3 deficiency enhanced the activation of macrophages and increased atherosclerotic lesions in LDLR-/- mice.

Increased Interleukin-11 Levels Are Correlated with Cardiac Events in Patients with Chronic Heart Failure.

Background: Interleukin-11 (IL-11) is an important inflammatory cytokine and has been demonstrated to participate in cardiovascular diseases. However, there have been no studies about the role of IL-11 in heart failure (HF). The present study is aimed at investigating whether IL-11 levels are associated with the cardiac prognosis in patients with HF.

Thrombospondin 1 Is Increased in the Aorta and Plasma of Patients With Acute Aortic Dissection.

Background: Previous studies have shown that thrombospondin 1 (TSP-1) is involved in cardiovascular diseases, such as atherosclerosis and abdominal aortic aneurysm. However, TSP-1 expression levels in human aortic dissection (AD) remain unknown.

Methods: TSP-1 levels were detected in aortas collected from control subjects and AD patients.

Sestrin2 increases in aortas and plasma from aortic dissection patients and alleviates angiotensin II-induced smooth muscle cell apoptosis via the Nrf2 pathway.

Background: Previous studies have demonstrated that oxidative stress is closely related to aortic dissection (AD). Sestrin2 (Sesn2) is an important antioxidant protein, and this study aimed to investigate whether Sesn2 participates in AD and the possible mechanisms.

Methods: Sesn2 expression was detected in aortas collected from AD patients and normal donors.