Global trends in research on oxidative stress related to heart failure from 2012 to 2021: a bibliometric analysis and suggestion to researchers.

Background: Oxidative stress leads to an increase in reactive oxygen in the body. During heart failure (HF), when the body's antioxidant defense system fails to remove excessive reactive oxygen species, myocardial cells will be damaged or even die. Over the past ten years, the number of research publications on oxidative stress related to HF has increased. Methods: We searched publications published in 2012-2021 and the Web of Science Core Collection (WoSCC) recording information. Based on the VOSviewer and CiteSpace, we conducted a bibliometric analysis of the overall distribution of journals, keywords, authors, major countries, annual output, active institutions, and cocited literature. The Global Citation Score (GCS) was used to evaluate the impact and quality of highly cited papers. Results: We retrieved 5,616 articles and reviews. Over the past ten years, the number of annual publications on oxidative stress related to HF has increased. USA has published the largest number of articles and obtained the highest number of citations (NC) and H-index. The University of California and PLoS One are the most productive affiliations and journals in terms of publications on oxidative stress related to HF. The GCS of articles written by Paulus WJ in 2013 was 1,632, which was the top ranking. The most frequent keywords are "oxidative stress", "heart failure", "inflammation", "dysfunction" and "apoptosis". The top three authors are Kang Yuming, Ren Jun and Okoshi Katashi. "Impact", "induced myocardial infarction", "cardiovascular outcome", "empagliflozin", "sglt2 inhibitor", "protect", and "Na+/H+ exchanger" have become popular research topics. Conclusions: Our research shows the research focus and development trends of oxidative stress related to HF in the past decade. Understanding the most important indicators of oxidative stress related to HF and the hot spots in the field of oxidative stress research related to HF can assist scholars, countries and policy-makers in the field in better understanding oxidative stress related to HF and can also lead to better decisions in oxidative stress treatment.

HIGD­1B inhibits hypoxia­induced mitochondrial fragmentation by regulating OPA1 cleavage in cardiomyocytes.

The dynamic regulation of mitochondrial morphology is key for eukaryotic cells to manage physiological challenges. Therefore, it is important to understand the molecular basis of mitochondrial dynamic regulation. The aim of the present study was to explore the role of HIG1 hypoxia inducible domain family member 1B (HIGD­1B) in hypoxia­induced mitochondrial fragmentation. Protein expression was determined via western blotting. Immunofluorescence assays were performed to detect the subcellular location of HIGD­1B. Cell Counting Kit­8 assays and flow cytometry were carried out to measure cell viability and apoptosis, respectively. Protein interactions were evaluated by co­immunoprecipitation. In the present study, it was found that HIGD­1B serves a role in cell survival by maintaining the integrity of the mitochondria under hypoxic conditions. Knockdown of HIGD­1B promoted mitochondrial fragmentation, while overexpression of HIGD­1B increased survival by preventing activation of caspase­3 and ­9. HIGD­1B expression was associated with cell viability and apoptosis in cardiomyocytes. Furthermore, HIGD­1B delayed the cleavage process of optic atrophy 1 (OPA1) and stabilized mitochondrial morphology by interacting with OPA1. Collectively, the results from the present study identified a role for HIGD­1B as an inhibitor of the mitochondrial fission in cardiomyocytes.

Identifying Type 2 Diabetic Brains by Investigating Disease-Related Structural Changes in Magnetic Resonance Imaging.

Diabetes with high blood glucose levels may damage the brain nerves and thus increase the risk of dementia. Previous studies have shown that dementia can be reflected in altered brain structure, facilitating computer-aided diagnosis of brain diseases based on structural magnetic resonance imaging (MRI). However, type 2 diabetes mellitus (T2DM)-mediated changes in the brain structures have not yet been studied, and only a few studies have focused on the use of brain MRI for automated diagnosis of T2DM. Hence, identifying MRI biomarkers is essential to evaluate the association between changes in brain structure and T2DM as well as cognitive impairment (CI). The present study aims to investigate four methods to extract features from MRI, characterize imaging biomarkers, as well as identify subjects with T2DM and CI.