Jiangtang decoction (JTD) is a China patented drug which contains Euphorbia humifusa Willd, Salvia miltiorrhiza Bunge, Astragalus mongholicus Bunge, Anemarrhena asphodeloides Bunge, and Coptis chinensis Franch. For decades, it has also been used clinically to treat diabetic nephropathy (DN) effectively; however, the associated mechanisms remain unknown. Thus, the present study aimed to examine the protective efficacy of JTD in DN and elucidate the underlying molecular mechanisms. A diabetic model using KK-Ay mice received a daily administration of JTD for 12 weeks. Body weight, blood glucose, triglycerides (TGs), total cholesterol (TC), urea nitrogen (UN), creatinine (Cr), and microalbumin/urine creatinine (MA/UCREA) was measured every 4 weeks. Furthermore, on the day of the sacrifice, blood, urine, and kidneys were collected to assess renal function according to general parameters. Pathological staining was performed to evaluate the protective renal effect of JTD. In addition, the levels of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin [IL]-6 and intercellular adhesion molecule [ICAM]-1), insulin receptor substrate [IRS]-1, advanced glycation end products [AGEs], and receptor of glycation end products [RAGE] were assessed. Finally, the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway and involvement of nuclear factor-κB (NF-κB) was further analyzed. After 12 weeks of metformin and JTD administration, the mice exhibited a significant amelioration in glucose and lipid metabolism dysfunction, reduced morphological changes in the renal tissue, decreased urinary albumin excretion, and normalized creatinine clearance. JTD treatment also reduced the accumulation of AGEs and RAGE, up-regulated IRS-1, and increased the phosphorylation of both PI3K (p85) and Akt, indicating that the activation of the PI3K/Akt signaling pathway was involved. Additionally, JTD administration reduced the elevated levels of renal inflammatory mediators and decreased the phosphorylation of NF-κB p65. These results demonstrate that JTD might reduce inflammation in DN through the PI3K/Akt and NF-κB signaling pathways.

Although significant progress has been made in developing preclinical models for metabolic dysfunction‐associated steatotic liver disease (MASLD), few have encapsulated the essential biological and clinical outcome elements reflective of the human condition. We conducted a comprehensive literature review of English‐language original research articles published from 1990 to 2023, sourced from PubMed, Embase, and Web of Science, aiming to collate studies that provided a comparative analysis of physiological, metabolic, and hepatic histological characteristics between MASLD models and control groups. The establishment of a robust metabolic dysfunction‐associated steatotic liver rodent model hinges on various factors, including animal species and strains, sex, induction agents and methodologies, and the duration of induction. Through this review, we aim to guide researchers in selecting suitable induction methods and animal species for constructing preclinical models aligned with their specific research objectives and laboratory conditions. Future studies should strive to develop simple, reliable, and reproducible models, considering the model's sensitivity to factors such as light–dark cycles, housing conditions, and environmental temperature. Additionally, the potential of diverse in vitro models, including 3D models and liver organ technology, warrants further exploration as valuable tools for unraveling the cellular mechanisms underlying fatty liver disease.

Anthracyclines represent a highly efficacious class of chemotherapeutic agents employed extensively in antitumor therapy. They are universally recognized for their potency in treating diverse malignancies, encompassing breast cancer, gastrointestinal tumors, and lymphomas. Nevertheless, the accumulation of anthracyclines within the body can lead to significant cardiac toxicity, adversely impacting both the survival rates and quality of life for tumor patients. This limitation somewhat restricts their clinical utilization. Determining how to monitor and mitigate their cardiotoxicity at an early stage has become an urgent clinical problem to be solved. Therefore, this paper reviews the mechanism of action, early monitoring, and strategies for the prevention of anthracycline-induced cardiotoxicity for clinical reference.

Protein post-translational modifications (PTMs), serving as crucial molecular switches regulating protein function and signaling pathways, have emerged as a research hotspot for elucidating the pathogenesis of Ischemic heart disease (IHD) and devising targeted therapeutic approaches. This review provides a comprehensive overview of the principal PTM types associated with IHD, encompassing phosphorylation, acetylation, ubiquitination, SUMOylation, glycosylation, lactylation and succinylation. It also delves into the molecular mechanisms and key targets of PTMs in IHD pathology, primarily involving myocardial energy metabolism, calcium homeostasis, inflammatory responses, cell death, and myocardial fibrosis. Additionally, this paper evaluates the prospective applications of specific kinase modulators, PTM-targeting modifiers, and gene editing technologies in the treatment of IHD, and proposes a "modificatomics"-oriented precision intervention strategy, which offers a novel perspective for the management of IHD.

1. Aortic stenosis is one of the most common valvular heart diseases in elderly populations, with a prevalence of moderate-to-severe disease reaching over 3% in individuals aged ≥75 years [1,2]. Ch...