MG53/TRIM72: multi-organ repair protein and beyond.

MG53, a member of the tripartite motif protein family, possesses multiple functionalities due to its classic membrane repair function, anti-inflammatory ability, and E3 ubiquitin ligase properties. Initially recognized for its crucial role in membrane repair, the therapeutic potential of MG53 has been extensively explored in various diseases including muscle injury, myocardial damage, acute lung injury, and acute kidney injury. However, further research has revealed that the E3 ubiquitin ligase characteristics of MG53 also contribute to the pathogenesis of certain conditions such as diabetic cardiomyopathy, insulin resistance, and metabolic syndrome. Moreover, recent studies have highlighted the anti-tumor effects of MG53 in different types of cancer, such as small cell lung cancer, liver cancer, and colorectal cancer; these effects are closely associated with their E3 ubiquitin ligase activities. In summary, MG53 is a multifunctional protein that participates in important physiological and pathological processes of multiple organs and is a promising therapeutic target for various human diseases. MG53 plays a multi-organ protective role due to its membrane repair function and its exertion of anti-tumor effects due to its E3 ubiquitin ligase properties. In addition, the controversial aspect of MG53's E3 ubiquitin ligase properties potentially causing insulin resistance and metabolic syndrome necessitates further cross-validation for clarity.

Collagen code in tumor microenvironment: Functions, molecular mechanisms, and therapeutic implications.

The tumor microenvironment (TME) is crucial in cancer progression, and the extracellular matrix (ECM) is an important TME component. Collagen is a major ECM component that contributes to tumor cell infiltration, expansion, and distant metastasis during cancer progression. Recent studies reported that collagen is deposited in the TME to form a collagen wall along which tumor cells can infiltrate and prevent drugs from working on the tumor cells. Collagen-tumor cell interaction is complex and requires the activation of multiple signaling pathways for biochemical and mechanical signaling interventions. In this review, we examine the effect of collagen deposition in the TME on tumor progression and discuss the interaction between collagen and tumor cells. This review aims to illustrate the functions and mechanisms of collagen in tumor progression in the TME and its role in tumor therapy. The findings indicated collagen in the TME appears to be a better target for cancer therapy.

Targeting cancer cachexia: Molecular mechanisms and clinical study.

Cancer cachexia is a complex systemic catabolism syndrome characterized by muscle wasting. It affects multiple distant organs and their crosstalk with cancer constitute cancer cachexia environment. During the occurrence and progression of cancer cachexia, interactions of aberrant organs with cancer cells or other organs in a cancer cachexia environment initiate a cascade of stress reactions and destroy multiple organs including the liver, heart, pancreas, intestine, brain, bone, and spleen in metabolism, neural, and immune homeostasis. The role of involved organs turned from inhibiting tumor growth into promoting cancer cachexia in cancer progression. In this review, we depicted the complicated relationship of cancer cachexia with the metabolism, neural, and immune homeostasis imbalance in multiple organs in a cancer cachexia environment and summarized the treatment progress in recent years. And we discussed the molecular mechanism and clinical study of cancer cachexia from the perspective of multiple organs metabolic, neurological, and immunological abnormalities. Updated understanding of cancer cachexia might facilitate the exploration of biomarkers and novel therapeutic targets of cancer cachexia.

[Pollution characteristics and ecological risk assessment of heavy metals in the surface sediments of the Yangtze River].

The concentrations of Cr, Co, Ni, Cu, Zn, Pb, Cd, As and Hg in surface sediment samples of Yangtze River collected in 2007 were analyzed and evaluated. The results indicated that the concentrations of Cu, Zn, Pb, Cd, As and Hg were significantly higher than those measured in 1990s. Principal component analysis showed that the cumulative proportion of the first three components accounted for 86.75% of the total variable, indicating the three major sources of heavy metals were industrial and mining wastewater, weathering and erosion of rocks, and urban electroplating industry wastewater and natural sources. Geoaccumulation index (Igeo) and enrichment factors (EF) also showed that the surface sediments of the Yangtze River were not contaminated with Cr, Co and Ni, lightly contaminated with Cu, Zn, As and Hg, and majorly contaminated with Ph and Cd. The ecological hazards for the heavy metals in the sediments were evaluated with the Hakanson ecological risk index. It was concluded the ecological hazards for each metal in a descending order were Cd > Hg > As > Zn > Pb > Cu > Co > Ni > Cr. The comprehensive index of potential ecological risks for metals indicated that 36% of the 61 sites had moderate potential ecological risks. Three sites had a high potential ecological risk, namely, Chongqing site of the main Yangtze River, Zishui Dongting Lake and Xinjiang site, whereas Xiangjiang Hengyang section, Xiangjiang Zhuzhou section, Xiangjiang Dongting Lake entrance, Dongting Lake and Shunan River belonged to the areas with extremely high potential ecological risk.