Cardiovascular disease (CVD) refers to a group of diseases involving the heart or blood vessels and is currently the leading cause of morbidity and mortality in many countries around the world and poses a serious economic burden. Macrophages are key effectors of inflammatory and innate immune responses, and their aberrant expression contributes to the development of various types of CVD.This study retrieved articles published from 1990-2022 on macrophages in CVD from the Web of Science core collection, based on CiteSpace and VOSviewer on these literature The annual output, countries and regions, institutions, authors, core journals, keywords and co-cited literature were analyzed. A total of 7,197 articles and reviews were retrieved, with a general upward trend despite slight fluctuations in annual publications. Europe, the United States and Asia are the main countries and regions publishing articles, especially the United States, with the highest number of articles (2,581), citations (173,692) and H-index (197), which also has the world's largest number of elite institutions, professional The country also has the world's largest number of elite institutions, professional researchers and high-impact journals, and is the leading country in this field of research. Keywords "inflammation", "immunology", "autophagy", "lipid-peroxidation" are the main pathogenesis of CVD caused by macrophages. "NLRP3", "nf kappa b" and "TNF-α" are the most frequently studied signalling pathways. Atherosclerosis, myocarditis and myocardial injury are the most studied disease types in this field. In addition, the study of macrophage-related CVD induced by COVID-19 seems to be a recent hot topic, and the mechanisms involved are mainly macrophage polarization, inflammatory factor storm, ACE2 and so on. The present study reveals hot spots and new trends in research on macrophages in CVD, which can provide scholars with key information in this field of research and help further explore new research directions.

Cardio-oncology has grown rapidly worldwide as an emerging interdisciplinary discipline over the past decade. In the present bibliometric review, we employed VOSviewer and Citespace software to describe the literature landscape concerning cardio-oncology from 2010 to 2022. As a result, a total of 1,194 relevant publications were identified in the Web of Science database with an increasing trend. The United States dominated the field during the research period, and Italy, England and Canada had emerged as significant contributors to the study. Ky. Bonnie, Herrmann. Joerg and Fradley. Michael G were the most productive researchers. JACC: CardioOncology was the journal dedicated to the discipline of cardio-oncology and had published the greatest number of papers. Vascular disease and atrial fibrillation have attracted much attention as the main cardiovascular burden. Immune checkpoint inhibitor-specific cardiovascular toxicity, biomarkers and imaging examination together with the prevention of cardio-oncology are potential research hotspots. Notably, basic research is lagging behind, for which more researches are needed to fill the gap. In conclusion, bibliometric analysis provided valuable information for the development of cardio-oncology, which is full of opportunities and challenges.

The crosstalk between the heart and kidney is carried out through various bidirectional pathways. Cardiorenal syndrome (CRS) is a pathological condition in which acute or chronic dysfunction in the heart or kidneys induces acute or chronic dysfunction of the other organ. Complex hemodynamic factors and biochemical and hormonal pathways contribute to the development of CRS. In addition to playing a critical role in generating metabolic energy in eukaryotic cells and serving as signaling hubs during several vital processes, mitochondria rapidly sense and respond to a wide range of stress stimuli in the external environment. Impaired adaptive responses ultimately lead to mitochondrial dysfunction, inducing cell death and tissue damage. Subsequently, these changes result in organ failure and trigger a vicious cycle. In vitro and animal studies have identified an important role of mitochondrial dysfunction in heart failure (HF) and chronic kidney disease (CKD). Maintaining mitochondrial homeostasis may be a promising therapeutic strategy to interrupt the vicious cycle between HF and acute kidney injury (AKI)/CKD. In this review, we hypothesize that mitochondrial dysfunction may also play a central role in the development and progression of CRS. We first focus on the role of mitochondrial dysfunction in the pathophysiology of HF and AKI/CKD, then discuss the current research evidence supporting that mitochondrial dysfunction is involved in various types of CRS.

Cardiorenal syndrome (CRS) is a state of coexisting heart failure and renal insufficiency in which acute or chronic dysfunction of the heart or kidney lead to acute or chronic dysfunction of the other organ.It was found that renal fibrosis is an important pathological process in the progression of type 2 CRS to end-stage renal disease, and progressive renal impairment accelerates the deterioration of cardiac function and significantly increases the hospitalization and mortality rates of patients. Previous studies have found that Hemodynamic Aiteration, RAAS Overactivation, SNS Dysfunction, Endothelial Dysfunction and Imbalance of natriuretic peptide system contribute to the development of renal disease in the decompensated phase of heart failure, but the exact mechanisms is not clear. Therefore, in this review, we focus on the molecular pathways involved in the development of renal fibrosis due to heart failure and identify the canonical and non-canonical TGF-β signaling pathways and hypoxia-sensing pathways, oxidative stress, endoplasmic reticulum stress, pro-inflammatory cytokines and chemokines as important triggers and regulators of fibrosis development, and summarize the therapeutic approaches for the above signaling pathways, including SB-525334 Sfrp1, DKK1, IMC, rosarostat, 4-PBA, etc. In addition, some potential natural drugs for this disease are also summarized, including SQD4S2, Wogonin, Astragaloside, etc.