C1q tumor necrosis factor‑related proteins (CTRPs), which are members of the adipokine superfamily, have gained significant interest in the recent years. CTRPs are homologs of adiponectin with numerous functions and are closely associated with metabolic diseases, such as abnormal glucose and lipid metabolism and diabetes. Previous studies have demonstrated that CTRPs are highly involved in the regulation of numerous physiological and pathological processes, including glycolipid metabolism, protein kinase pathways, cell proliferation, cell apoptosis and inflammation. CTRPs also play important roles in the development and progression of numerous types of tumor, including liver, colon and lung cancers. This observation can be attributed to the fact that diabetes, obesity and insulin resistance are independent risk factors for tumorigenesis. Numerous CTRPs, including CTRP3, CTRP4, CTRP6 and CTRP8, have been reported to be associated with tumor progression by activating multiple signal pathways. CTRPs could therefore be considered as diagnostic markers and therapeutic targets in some cancers. However, the underlying mechanisms of CTRPs in tumorigenesis remain unknown. The present review aimed to determine the roles and underlying mechanisms of CTRPs in tumorigenesis, which may help the development of novel cancer treatments in the future.

Background: Coronary heart disease (CHD) is one of the most common causes of morbidity and mortality in type 2 diabetes mellitus (T2DM). Oxidative stress is one of the important contributors to the pathogenesis of CHD. Sestrin2 is a stress-induced antioxidant protein that plays a important role in T2DM and CHD. However, the relationship between serum Sestrin2 levels and T2DM with CHD remains unclear.Aim: This study aimed to investigate the relationship between serum Sestrin2 levels and CHD in patients with type 2 diabetes.Methods: A total of 70 T2DM patients with CHD and 69 T2DM patients were enrolled in this study. Clinical features and metabolic indices were identified. Serum Sestrin2 was measured by ELISA.Results: Serum Sestrin2 levels in T2DM-CHD groups were significantly lower compared with the T2DM group (11.17 (9.79, 13.14) ng/mL vs 9.46 (8.34, 10.91) ng/mL). Bivariate correlation analysis revealed that serum Sestrin2 levels were negatively correlated with age (r = − 0.256,P = 0.002), BMI (r = − 0.206,P = 0.015), FBG (r = − 0.261,P = 0.002) and Tyg index (r = − 0.207,P < 0.014). Binary logistic regression suggested that low serum Sestrin2 levels were related to the increased risk of T2DM-CHD (P < 0.05). In addition, the receiver operating characteristic analysis revealed that the area under the curve of Sestrin2 was 0.724 (95% CI 0.641–0.808,P < 0.001) to predict T2DM-CHD patients (P < 0.001).Conclusion: The Sestrin2 levels were highly associated with CHD in diabetes patients. Serum Sestrin2 may be involved in the occurrence and development of diabetic with CHD.

Object. L6 cells were cultured to explore the possible mechanism underlying the improvement of insulin resistance by Liraglutide (LR). Methods. Cells were divided into 5 groups—control, high‐fat, 10 nmol/L LR + 0.6 mmol/L palmitic acid (PA) (10LR), 100 nmol/L LR + 0.6 mmol/L PA (100LR), and 1000 nmol/L LR + 0.6 mmol/L PA (1000LR). CCK‐8 method to detect cell viability, GPO‐PAP enzymatic method to detect intracellular triglyceride content, and reverse transcription quantitative real‐time polymerase chain reaction (RT‐qPCR) and western blotting methods to detect fatty acid translocase CD36 (FAT/CD36) and fatty acid binding protein 4 (FABP4) in L6 cells, glucose‐regulated protein 78 (GRP78), glucose transporter 4 (GLUT4) expression at the mRNA and protein levels, respectively, were performed. Results. We found that after PA intervention for 24 h, the cell viability decreased significantly; the cell viability of the LR group was higher than that of the high‐fat group (P < 0.01). After PA intervention, compared with those in the high‐fat group, GRP‐78, FAT/CD36, FABP4 mRNA ((4.36 ± 0.32 vs. 8.15 ± 0.35); (1.00 ± 0.04 vs. 2.46 ± 0.08); (2.88 ± 0.55 vs. 8.29 ± 0.52), P < 0.01) and protein ((3338.13 ± 333.15 vs. 4963.98 ± 277.29); (1978.85 ± 124.24 vs. 2676.07 ± 100.64); (3372.00 ± 219.84 vs. 6083.20 ± 284.70), both P < 0.01) expression decreased in the LR group. The expression levels of GLUT4 mRNA ((0.75 ± 0.04 vs. 0.34 ± 0.03), P < 0.01) and protein ((3443.71 ± 191.89 vs. 2137.79 ± 118.75), P < 0.01) increased. Conclusion. Therefore, we conclude that LR can reverse PA‐induced cell inactivation and lipid deposition, which may be related to the change in GRP‐78, FAT/CD36, FABP4, GLUT4, and other factors.

This review examines the mechanisms of left ventricular dysfunction, focusing on the interplay between ventricular remodeling, autophagy, and mitochondrial dysfunction following myocardial infarction. Left ventricular dysfunction directly affects the heart’s pumping efficiency and can lead to severe clinical outcomes, including heart failure. After myocardial infarction, the left ventricle may suffer from weakened contractility, diastolic dysfunction, and cardiac remodeling, progressing to heart failure. Thus, this article discusses the pathophysiological processes involved in ventricular remodeling, including the injury and repair of infarcted and non-infarcted myocardia, adaptive changes, and specific changes in left ventricular systolic and diastolic functions. Furthermore, the role of autophagy in maintaining cellular energy homeostasis, clearing dysfunctional mitochondria, and the key role of mitochondrial dysfunction in heart failure is addressed. Finally, this article discusses therapeutic strategies targeting mitochondrial dysfunction and enhancing mitophagy, providing clinicians and researchers with the latest insights and future research directions.

Tumors of the digestive system have always received attention, and their occurrence and development are regulated by various mechanisms such as inflammation and immunity, glucose and lipid metabolism, and tumor angiogenesis. Complement Clq/TNF‑related protein 6 (CTRP6) is a member of the CTRP family; it is widely expressed in various tissues and cell types, and plays a biological role in a number of mechanisms, such as glucose and lipid metabolism and inflammation. Recent studies have revealed the tumor‑promoting effect of CTRP6 in gastric cancer, liver cancer, colorectal cancer and other gastrointestinal tumors, but, to the best of our knowledge, there has been no systematic discussion on the tumor‑promoting mechanism of CTRP6. The present study reviews the role of CTRP6 in tumors of the digestive system and its possible mechanisms.

Despite not showing substantial stenosis of coronary arteries, Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA) presents with myocardial ischemia injury, thus having a grave prognosis and a high risk of long-term complications. This necessitates increased clinical attention and exploration of its root causes to prevent a similar crisis. Research on MINOCA is limited, especially in terms of its clinical attributes, long-term outlook, risk stratification, and prognosis-linked cardiometabolic risk factors. This review aims to fill these gaps, providing an extensive overview of clinical trials and studies on MINOCA to separate the issue from the presence of non-obstructive coronary arteries in cardiac patients. It has been found that MINOCA patients still face a high risk of long-term adverse events. Due to social and physiological factors, the hospital mortality rate is higher among women, and they are also more susceptible to MINOCA. Cardiac metabolic risk factors, including disorder of glucose and lipid metabolism, as well as changes in serum CysC levels, have significant impacts on the occurrence and prognosis of MINOCA. Further research is still needed to fully understand the complex biological mechanisms underlying the prognostic factors of MINOCA. A profound understanding of these factors could reveal potential targets for improving prognosis, thereby indicating new strategies for managing this cardiovascular condition.