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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.

Pathological cardiac remodeling normally involves changes in structure, function, and energy metabolism of the heart induced by cardiac injury or load, terminally leading to heart failure. Cardiac remodeling plays an essential role in the progression of cardiovascular disease, thus increasingly identified as an important therapeutic target for heart failure of all pathogenesis. Puerarin, as a natural isoflavone mainly from Pueraria lobata （Willd.）Ohwi, has been developed as injections, eye drops, microemulsions, etc., and is widely used in the clinical treatment of cardiovascular diseases in eastern Asia countries. In recent years, a growing number of studies have shown that puerarin significantly inhibits myocardial hypertrophic growth, myocyte death, fetal gene expression, fibroblast proliferation and activation, improves energy metabolism, promotes post-infarction angiogenesis, and suppresses inflammation and oxidative stress, consequently attenuating or preventing cardiac remodeling in response to multiple stimuli ( e.g., pressure overload, MIRI, MI, Iso, and Ang II stimulation). This review summarized the roles and underlying molecular mechanisms of puerarin in cardiac remodeling induced by diverse etiologies, aiming to help develop novel therapeutic strategies to prevent or reverse pathological ventricular remodeling.

Diabetic kidney disease (DKD) is a major global public health concern due to its high prevalence and mortality, and high healthcare cost. Conventional Western therapies for DKD fail to provide favourable efficacy. Chinese medicine (CM) has been widely used to combat DKD in China and other Asian countries. The clinical effects and mechanism of CM in treating DKD have not been fully elucidated. This review summarizes current knowledge of CM therapeutic modalities for DKD, especially Chinese herbal medicine (CHM), and potential mechanisms.

Tubular injury is closely correlated with the development of progressive diabetic nephropathy (DN), particularly in cases of type 2 diabetes. The apoptosis of tubular cells has been recognized as a major cause of tubular atrophy, followed by tubulointerstitial fibrosis. Electron transfer flavoprotein β (ETFβ) is known as an important electron acceptor in energy metabolism, but its role in DN was not fully understood. In the present study, we examined the expression pattern of ETFβ using diabetic kidney samples and further investigated ETFβ involvement in tubular epithelial cell (TEC) apoptosis. Human renal biopsy specimens from patients with DN as well as a spontaneous rat model of diabetes using Otsuka Long-Evans Tokushima fatty (OLETF) rats, were employed in order to examine the expression of ETFβ and cell apoptosis in kidneys during the development of DN (for the rats, at 36 and 56 weeks of age respectively). Moreover, ETFβ siRNA was used to investigate the role of ETFβ in the apoptosis of renal tubular cells. Our present results showed that the expression of ETFβ in the kidneys was progressively decreased both in patients with DN and OLETF rats, which coincided with progressive renal injury and TEC apoptosis. In addition, the in vitro study demonstrated that knockdown of ETFβ caused apoptosis in tubular cells, as proven by the increased expression of pro‑apoptotic proteins and TUNEL assay. Therefore, the findings of our present study suggest that ETFβ plays an important role in renal tubular cell apoptosis during the progression of DN.

Background Diabetic kidney disease (DKD) is one of the most common microvascular complications of diabetes mellitus and the main cause of end-stage renal disease. Present medications for DKD are not entirely satisfactory. Preliminary studies indicate that the Chinese herbal formula Tangshen Formula (TSF) appears to decrease the proteinuria and improve the estimated glomerular filtration rate (eGFR) in DKD patients. Methods/design This trial is a five-center, randomized, double-blind, placebo-controlled study. DKD patients with a 24-h urinary protein (24 h UP) level between 0.5 and 3.5 g and serum creatinine