LncRNA Meg3 Aggravates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Rats by Activating the Hedgehog Pathway.

Background: The hedgehog signaling pathway exerts vital functions in regulating epithelial-to-mesenchymal transition (EMT) in renal interstitial fibrosis (RIF). It was reported that lncRNA-maternally expressed gene 3 (lncRNA Meg3) can regulate hepatic fibrosis by regulating the expression of smoothened (Smo) in the hedgehog signaling pathway. However, the specific role of lncRNA Meg3 in renal fibrosis resulting from unilateral ureteral obstruction (UUO) by regulating the hedgehog signaling pathway has not been reported.

The aryl hydrocarbon receptor in immune regulation and autoimmune pathogenesis.

As a ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR) is activated by structurally diverse ligands derived from the environment, diet, microorganisms, and metabolic activity. Recent studies have demonstrated that AhR plays a key role in modulating both innate and adaptive immune responses. Moreover, AhR regulates innate immune and lymphoid cell differentiation and function, which is involved in autoimmune pathogenesis.

Sublytic C5b-9 Induces CCL3/4 Production and Macrophage Accumulation in Thy-1N Rats via PKC-α/p65/IRF-8 Axis.

Mesangioproliferative glomerulonephritis (MsPGN) is a common human kidney disease. Rat Thy-1 nephritis (Thy-1N) is an animal model widely used for the study of MsPGN. Thy-1N is not only sublytic C5b-9-dependent, but also related to pro-inflammatory cytokine production and macrophage (Mφ) accumulation in rat renal tissues.

Roles of IL-25 in Type 2 Inflammation and Autoimmune Pathogenesis.

Interleukin-17E (IL-25) is a member of the IL-17 cytokine family that includes IL-17A to IL-17F. IL-17 family cytokines play a key role in host defense responses and inflammatory diseases. Compared with other IL-17 cytokine family members, IL-25 has relatively low sequence similarity to IL-17A and exhibits a distinct function from other IL-17 cytokines.

Adiponectin Enhances B-Cell Proliferation and Differentiation Activation of Akt1/STAT3 and Exacerbates Collagen-Induced Arthritis.

Although B cells have been shown to contribute to the pathogenesis of rheumatoid arthritis (RA), the precise role of B cells in RA needs to be explored further. Our previous studies have revealed that adiponectin (AD) is expressed at high levels in inflamed synovial joint tissues, and its expression is closely correlated with progressive bone erosion in patients with RA. In this study, we investigated the possible role of AD in B cell proliferation and differentiation.

Overexpression of long noncoding RNA ANRIL inhibits phenotypic switching of vascular smooth muscle cells to prevent atherosclerotic plaque development .

Background: Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a key role in atherosclerosis. Long noncoding RNA ANRIL (lncRNA-ANRIL) is critical in vascular homeostasis. Metformin produces multiple beneficial effects in atherosclerosis.

IL-17 sustains the plasma cell response via p38-mediated Bcl-xL RNA stability in lupus pathogenesis.

Recent studies have demonstrated a central role for plasma cells in the development of autoimmune diseases, such as systemic lupus erythematosus (SLE). Currently, both the phenotypic features and functional regulation of autoreactive plasma cells during SLE pathogenesis remain largely unclear. In this study, we first found that a major subset of IL-17 receptor-expressing plasma cells potently produced anti-dsDNA IgG upon IL-17A (IL-17) stimulation in SLE patients and lupus mice.

Effects of prostaglandin E combined with continuous renal replacement therapy on septic acute kidney injury.

Background: The effects of prostaglandin E (PGE) combined with continuous renal replacement therapy (CRRT) on renal function and inflammatory responses in patients with septic acute kidney injury (SAKI) remain unclear.

Aim: To investigate the effects of PGE combined with CRRT on urinary augmenter of liver regeneration (ALR), urinary Na+/H+ exchanger 3 (NHE3), and serum inflammatory cytokines in patients with SAKI.

Methods: The clinical data of 114 patients with SAKI admitted to Yichang Second People's Hospital from May 2017 to January 2019 were collected.

The Roles of Immune Cells in the Pathogenesis of Fibrosis.

Tissue injury and inflammatory response trigger the development of fibrosis in various diseases. It has been recognized that both innate and adaptive immune cells are important players with multifaceted functions in fibrogenesis. The activated immune cells produce various cytokines, modulate the differentiation and functions of myofibroblasts via diverse molecular mechanisms, and regulate fibrotic development.

Aliskiren Improved the Endothelial Repair Capacity of Endothelial Progenitor Cells from Patients with Hypertension via the Tie2/PI3k/Akt/eNOS Signalling Pathway.

Background: Studies show that aliskiren exerts favourable effects not only on endothelial progenitor cells (EPCs) but also on endothelial function. However, the mechanism of the favourable effect of aliskiren on EPCs from patients with hypertension is unclear and remains to be further studied.

Methods: The object of this study was to investigate and assess the in vitro function of EPCs pretreated with aliskiren.

Endothelial progenitor cell impairment mediated vasodilation dysfunction via diminishing nitric oxide production in postmenopausal females.

Vascular endothelial dysfunction is the major contributing factor to hypertension. Endothelial progenitor cells (EPCs) are essential for endogenous vascular endothelial renovation. The activity and number of circulating EPCs are preserved in prehypertensive premenopausal females according to our previous research.

Attenuated endothelial function is associated with decreased endothelial progenitor cells and nitric oxide in premenopausal diabetic women.

Previous studies have demonstrated that the deleterious effect of diabetes mellitus (DM) on the risk of cardiovascular disease also occurs in premenopausal women, in spite of their relatively high estrogen levels; however, the underlying mechanism remains unclear. The present study aimed to investigate the sex‑related differences in circulating endothelial progenitor cells (EPCs) in a relatively young population with type 2 DM (T2DM) and its underlying mechanism. The number and functional activity of circulating EPCs, and vascular endothelial function assessed using flow‑mediated dilation (FMD), were compared in premenopausal women and age‑matched men with or without T2DM.

Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women.

Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism.

Cardiac magnetic resonance and galectin-3 level as predictors of prognostic outcomes for non-ischemic cardiomyopathy patients.

This study was aimed at determining whether late gadolinium enhancement (LGE) in conjunction with Galectin-3 (Gal-3) level offered more precise prognosis of non-ischemic cardiomyopathy (NICM) in comparison to LGE alone. Results of LGE and Gal-3 expression in 192 patients with NICM, including 85 subjects with dilated cardiomyopathy (DCM) and 107 with hypertrophic cardiomyopathy (HCM), were examined. As suggested by the characteristics of LGE and Gal-3 levels, patients were divided into four groups: LGE positive + low Gal-3 (n = 10 for DCM, n = 15 for HCM), LGE positive + high Gal-3 (n = 25 for DCM, n = 51 for HCM), LGE negative + low Gal-3 (n = 32 for DCM, n = 29 for HCM), LGE negative + high Gal-3 (n = 18 for DCM, n = 12 for HCM).

[Simultaneous transcatheter therapy for ventricular septal defect combined with atrial septal defect].

Objective: To access the possibility, methods and efficacy of simultaneous transcatheter therapy for ventricular septal defect ( VSD ) combined with atrial septal defect (ASD).

Methods: In 68 patients with VSD, four patients ranging from 3 to 24 years old were combined with ASD. The diameters of perimembranous VSD were 2 approximately 10.

[Therapeutic effect and safety of transcatheter occlusion of ventricular septal defects in 50 patients].

Objective: To determine the therapeutic effect and safety of transcatheter closure of ventricular septal defects (VSD) in 50 patients.

Methods: Fifty patients were diagnosed by transthoracic echocardiography. To perform the operation, transthoracic echocardiography and X ray were used continuously to monitor the procedure.

[Formation and function of coronary collateral circulation and their influencing factors].

Objective: To clarify the formation and function of coronary collateral circulation (CCC) in coronary artery disease (CAD) patients with severe coronary artery stenosis and their influencing factors.

Methods: Coronary angiography was performed on 266 CAD patients with severe coronary stenosis. CCC formation was evaluated by Rentrop rating on those 266 patients and 401 severe stenosis arteries; while in CCC formed patients, CCC function was evaluated by Werner collateral collection (CC) rating.