2023: A year of accomplishments for the 13 Science Citation Index Expanded- and Emerging Sources Citation Index-indexed journals.

In 2023, Baishideng Publishing Group () routinely published 47 open-access journals, including 46 English-language journals and 1 Chinese-language journal. Our successes were accomplished through the collective dedicated efforts of staffs, Editorial Board Members, and Peer Reviewers. Among these 47 journals, 7 are included in the Science Citation Index Expanded (SCIE) and 6 in the Emerging Sources Citation Index (ESCI).

Shenkang injection combined with alprostadil for chronic renal failure: A systematic review and meta-analysis.

Objective: To systematically evaluate the clinical efficacy and safety of Shenkang injection (SKI) combined with alprostadil in the treatment of chronic renal failure (CRF).

Method: Randomized controlled trials (RCTs) of Shenkang injection combined with alprostadil in CRF treatment were investigated by retrieving a total of 7 databases including CNKI, Wanfang database, VIP, CBM, PubMed, Embase and Cochrane Library, with the search time ranging from 2012 to now. Revman 5.

Substrate rigidity dictates colorectal tumorigenic cell stemness and metastasis via CRAD-dependent mechanotransduction.

Tumor physical microenvironment contributes greatly to the response of tumor cells. However, the mechanism of how extracellular substrate rigidity remodels colorectal cancer (CRC) cell fate and affects CRC progression remains elusive. Here, we show that F-actin regulator KIAA1211, also known as Capping protein inhibiting regulator of actin dynamics (CRAD), negatively correlates with CRC progression, stemness, and metastasis.

Left atrial diameter and atrial fibrillation, but not elevated NT-proBNP, predict the development of pulmonary hypertension in patients with HFpEF.

Background: The determinants of pulmonary hypertension (PH) due to heart failure with preserved ejection fraction (HFpEF) have been poorly investigated in patients with cardiovascular diseases (CVD).

Methods: From July 1 2017 to March 31 2019, a total of 149 consecutive HFpEF patients hospitalized with CVD were enrolled in this prospective cross-sectional study. A systolic pulmonary artery pressure (PASP) > 35 mmHg estimated by echocardiography was defined as PH-HFpEF.

Low shear stress induces endothelial cell apoptosis and monocyte adhesion by upregulating PECAM‑1 expression.

Low shear stress serves an important role in the initiation and progression of atherosclerotic lesions, with an impact on progression, but its detailed mechanisms are .not yet fully known. The present study aimed to investigate endothelial cell (EC) apoptosis, as well as monocyte adhesion induced by low shear stress and the potential underlying mechanisms.

Correction: Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Risks of incident heart failure with preserved ejection fraction in Chinese patients hospitalized for cardiovascular diseases.

Background: Endogenous aldehyde damages DNA and potentiates an ageing phenotype. The aldehyde dehydrogenase 2 () polymorphism has a prevalence of 30%-50% in Asian populations. In this study, we aimed to analyze risk factors contributing to the development of heart failure with preserved ejection fraction (HFpEF) along with the genetic exposure in Chinese patients hospitalized with cardiovascular diseases (CVD).

FoxO3 reverses 5-fluorouracil resistance in human colorectal cancer cells by inhibiting the Nrf2/TR1 signaling pathway.

5-fluorouracil (5-FU) is widely used in chemotherapy for colorectal cancer (CRC), but a high rate of chemoresistance reduces its effectiveness in clinical treatment. We found remarkably decreased expression of forkhead box 3 (FoxO3) protein, a tumor inhibitor, in 5-FU-resistant SW620 and HCT-8 (SW620/5-FU and HCT-8/5-FU) cells. Moreover, FoxO3 overexpression sensitized SW620/5-FU and HCT-8/5-FU cells to 5-FU.

Macrophage-derived CCL5 facilitates immune escape of colorectal cancer cells via the p65/STAT3-CSN5-PD-L1 pathway.

Infiltrated macrophages are an important constituent of the tumor microenvironment and play roles in tumor initiation and progression by promoting immune evasion. However, the molecular mechanism by which macrophage-derived cytokines foster immune escape of colorectal cancer (CRC) is unclear. Here, we demonstrated that macrophage infiltration induced by lipopolysaccharide (LPS) or a high-cholesterol diet (HCD) significantly promoted CRC growth.

Discovery of phosphonamidate IDO1 inhibitors for the treatment of non-small cell lung cancer.

Targeting indoleamine 2,3-dioxygenase 1 (IDO1) has been identified as an attractive approach for the development of cancer immunotherapy. In this study, a series of phosphonamidate ester containing compounds were designed, synthesized and evaluated for their inhibitory activities against IDO1. Among them, compounds 16, 17, and 26 with good IDO1 inhibitory (HeLa IDO1 IC = 10-21 nM, hIDO1 IC = 78-121 nM) activities were selected for further investigation and showed good physicochemical properties.

ALDH2 rs671 polymorphism and the risk of heart failure with preserved ejection fraction (HFpEF) in patients with cardiovascular diseases.

Aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism is an established genetic risk of hypertension, diabetes, and coronary heart diseases in Asian population. Previous experimental data showed ALDH2 regulated inflammation, a potential mechanism of heart failure with preserved ejection fraction (HFpEF). However, clinically, the association between ALDH2 polymorphism and incidence of HFpEF remains unknown.

Low shear stress induces vascular eNOS uncoupling via autophagy-mediated eNOS phosphorylation.

Uncoupled endothelial nitric oxide synthase (eNOS) produces O instead of nitric oxide (NO). Earlier, we reported rapamycin, an autophagy inducer and inhibitor of cellular proliferation, attenuated low shear stress (SS) induced O production. Nevertheless, it is unclear whether autophagy plays a critical role in the regulation of eNOS uncoupling.

Inhibition of angiotension II type 1 receptor reduced human endothelial inflammation induced by low shear stress.

Low shear stress (LSS)-induced endothelial inflammation is the basis for the development of atherosclerosis. However, the mechanism underlying LSS-induced inflammation is not well understood. The angiotensin II type 1 receptor (AT1R), a component of the renin-angiotensin system, participates in atherosclerotic plaque progression.

Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway.

Reactive oxygen species (ROS) contribute to many aspects of physiological and pathological cardiovascular processes. However, the underlying mechanism of ROS induction by low shear stress (LSS) remains unclear. Accumulating evidence has shown that the angiotensin II type 1 receptor (AT1R) is involved in inflammation, apoptosis, and ROS production.

Modulation of low shear stress‑induced eNOS multi‑site phosphorylation and nitric oxide production via protein kinase and ERK1/2 signaling.

Physiological shear stress has been demonstrated to serve an atheroprotective function by stimulating endothelial nitric oxide synthase (eNOS) multi‑site phosphorylation. Low shear stress (LSS) serves an atheroprone role by increasing endothelial cell apoptosis and inflammation. The present study assessed whether LSS inhibited nitric oxide (NO) production in human umbilical vein endothelial cells by modulating eNOS phosphorylation and potential signaling pathways.

Cardamonin Alleviates Pressure Overload-induced Cardiac Remodeling and Dysfunction Through Inhibition of Oxidative Stress.

Pressure overload-induced cardiac remodeling and dysfunction progress to heart failure, which is mainly due to excessive oxidative stress. Hence, our study aimed to illustrate whether cardamonin, a kind of chalcone, could attenuate maladaptive cardiac changes and ameliorate cardiac insufficiency through its antioxidant mechanism. In vivo, our study revealed that cardamonin treatment could attenuate transverse aortic contraction-induced cardiac remodeling and dysfunction.