Macrophage-specific autophagy-related gene HSPB8 is involved in the macrophage polarization in atherosclerosis.

BACKGROUND: Atherosclerosis (AS) is a chronic inflammatory disease, as a main cause leading to vascular diseases worldwide. Although increasing studies have focused on macrophages in AS, the exact relating mechanism is still largely unclear. Our study aimed to explore the pathogenic role and diagnostic role of macrophage autophagy related genes (MARGs) in AS. METHODS: All datasets were downloaded from Gene Expression Omnibus database and Human Autophagy Database. The differential expression analysis and cross analysis were performed to identify candidate MARGs. GO and KEGG enrichment analyses were conducted to obtain the functional information. Moreover, we analyzed the correlation between target gene and macrophage polarization in AS. The correlation between target gene and plaque instability, different stages of AS were also analyzed. RESULTS: Compared with normal samples, a total of 575 differentially expressed genes (DEGs) were identified in AS samples. A total of 12 overlapped genes were obtained after cross-analysis of the above 575 DEGs and autophagy related genes (ARGs). Then, 10 MARGs were identified in AS samples, which were significantly enriched in 22 KEGG pathways and 61 GO terms. The expression of HSPB8 was significantly down-regulated in atherosclerotic samples compared with normal samples (with largest fold change). Meanwhile, the proportion of M-CSF in low HSPB8 expression AS group was higher than high expression AS group. Furthermore, the expression of HSPB8 was negatively correlated with most inflammatory factors. CONCLUSION: The downregulation of MARG HSPB8 probably involves in the M2 macrophage polarization in AS samples. HSPB8 is a promising diagnostic marker for AS patients.

Global trends and frontiers in research on exercise training for heart failure: a bibliometric analysis from 2002 to 2022.

Background: Heart failure is a common cardiovascular disease that imposes a heavy clinical and economic burden worldwide. Previous research and guidelines have supported exercise training as a safe, effective, and cost-efficient treatment to intervene in heart failure. The aim of this study was to analyze the global published literature in the field of exercise training for heart failure from 2002 to 2022, and to identify hot spots and frontiers within this research field. Methods: Bibliometric information on literature on the topic of exercise training for heart failure published between 2002 and 2022 was searched and collected in the Web of Science Core Collection. CiteSpace 6.1.R6 (Basic) and VOSviewer (1.6.18) were applied to perform bibliometric and knowledge mapping visualization analyses. Results: A total of 2017 documents were retrieved, with an upward-stable trend in the field of exercise training for heart failure. The US authors were in the first place with 667 documents (33.07%), followed by Brazilian authors (248, 12.30%) and Italian authors (182, 9.02%). The Universidade de São Paulo in Brazil was the institution with the highest number of publications (130, 6.45%). The top 5 active authors were all from the USA, with Christopher Michael O'Connor and William Erle Kraus publishing the most documents (51, 2.53%). The International Journal of Cardiology (83, 4.12%) and the Journal of Applied Physiology (78, 3.87%) were the two most popular journals, while Cardiac Cardiovascular Systems (983, 48.74%) and Physiology (299, 14.82%) were the two most popular categories. Based on the results of keyword co-occurrence network and co-cited reference network, the hot spots and frontiers of research in the field of exercise training for heart failure were high-intensity interval training, behaviour therapy, heart failure with preserved ejection fraction, and systematic reviews. Conclusion: The field of exercise training for heart failure has experienced two decades of steady and rapid development, and the findings of this bibliometric analysis provide ideas and references for relevant stakeholders such as subsequent researchers for further exploration.

1,2,3,4,6­penta­O­galloyl­ß­D­glucose alleviates inflammation and oxidative stress in diabetic nephropathy rats through MAPK/NF­κB and ERK/Nrf2/HO­1 signaling pathways.

Diabetic nephropathy (DN) is one of the main causes of chronic renal failure, which is also the final cause of mortality in ~30% of diabetic patients. 1, 2, 3, 4, 6-penta-O-galloyl-ß-D-glucose (PGG) from Galla rhois has anti-inflammation, anti-oxidation and angiogenesis effects. The present study aimed to explore the protective effects on diabetic nephropathy rats by alleviating inflammation and oxidative stress and the underlying mechanism. High-fat diet/STZ induced rats and high glucose (HG) induced podocytes (MPC5) were used to simulate the DN in vivo and in vitro. The blood glucose level was measured using a blood glucose meter and renal function was determined by an automatic biochemical analyzer. The pathological changes and renal fibrosis were observed through hematoxylin and eosin, periodic acid-Schiff and Masson staining. The expression of nephrin in tissues, fibrosis-related proteins in tissues, MAPK/NF-κB and ERK/nuclear factor erythroid-derived 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway related proteins in tissues and apoptosis related proteins in tissues and podocytes was detected by western blotting. The inflammatory response and oxidative stress in tissues and podocytes were determined by respective commercial kits and apoptosis in tissues and podocytes was detected by TUNEL assay. The viability of podocytes treated with PGG with or without HG was analyzed by CCK-8 assay. As a result, the blood glucose level, urinary albumin/creatinine ratio, blood urea nitrogen and serum creatinine in blood were all increased and nephrin expression was decreased. The pathological changes and renal fibrosis were aggravated and the inflammation, oxidative stress and apoptosis in renal tissues were enhanced. The above effects were reversed by PGG treatment dose-dependently. MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways were activated in DN rats and were suppressed by PGG treatment. The reduced viability and increased apoptosis, inflammation and oxidative stress in MPC5 cells were shown in HG induction, which was reversed by PGG treatment. However, P79350 (p38 agonist) and LM22B-10 (ERK1/2 agonist) weakened the effect of PGG. In conclusion, PGG protects against DN kidney injury by alleviating inflammation and oxidative stress by suppressing the MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways.