research background

Cuproptosis represents a novel system of cell death, characterized by intracellular copper ion accumulation. Unlike other cell death passages, its unique process has created significant interest in the treatment of inflammatory bowel disease (IBD) and colorectal cancer (CRC) due to its promising applications. Emerging evidence suggests that copper metabolism and cupoptosis can play a dual regulatory role in pathological cellular environment, especially in modifying oxidative stress reactions, metabolic reprograming and immunotheraputic efficacy. The appropriate copper level can promote the progression of the disease and increase sympathetic effects, but beyond a certain range, copper disease can suppress the development of the disease by inducting copoptosis in cells. This makes a potential novel therapeutic goal for IBD and CRC to the level of disgraced copper.

This article highlights the dual role of copper metabolism and cuphoptosis in the progression of IBD and CRC, discovering possible applications of copper-based treatments in disease treatment. Additionally, it further explains the regulatory effects of tumor immune microelement on cuproptosis and establishes the medical capacity of the cupoptosis goal strategies to overcome traditional chemotherapy and resistance to emerging immunotherapy. This provides new research instructions for future development of cuproptosis inducers. Finally, the article discusses the latest progress in the latest genes and latest progresses in the latest genes in related genes for the treatment of future research preferences and unresolved questions, emphasizing the IBD and CRC.

Research progress

1. IBD and CRC binoculations of copper metabol

Studies have shown that copper metabolism and cuphoptosis displays dual effects in the pathological processes of IBD and CRC. As an essential trace element, copper homeostasis imbalance can lead to cell death, which contains copoptosis representing a newly identified copper -dependent cell death mechanism.

In IBD, copper affects intestinal obstruction function by regulating oxidative stress and immune reactions. For example, excessive copper increases oxidative stress and damages intestinal epithelial cells, while copper chelators can reduce Swelling By stopping the NF-κB route. In CRC, copper accelerates the progression of the disease by promoting angiogenies and tumor metastasis, yet cuphoptosis can kill selective tumor cells. These findings reveal the complex role of copper metabolism and copper in intestinal diseases.

2. Interaction between copoptosis and tumor immunity

Cuproptosis not only induces direct tumor cell death, but also re -prepares tumor immune microement (TME). Studies have found that copper complexes can induce nanoptosis (CU (i) np) cuproptosis and dendritic cell (DC) can release molecular patterns associated with damage by promoting maturity and CD8+ T cell infiltration.
In addition, copper ionophorus (eg, dysulfiram/copper complex) M1 increases anti-tumor immune responses by promoting the M1 macrophages polliation and pressing the PD-L1 expression. These findings suggest that copoptosis can potential existing immunotherapy through immune modulation, offering novel strategies to remove tumor resistance.

3. Clinical capacity of copper-targeted remedies

Copper metabolism -related proteins (including ATP 7A/B and FDX 1) have emerged as a potential therapeutic goals for CRC. Preclinical studies indicate that copper disciplines (eg, tetrathiomolibdate) and copper ionophorus (eg, dysulfiram) can prevent tumor growth by inducting copoptosis.

In addition, copper-based nanomedicine (eg, EC@Docs NPS) combined with chemotherapy or photothmal therapy has greatly enhanced the antitumor efficacy. In clinical trials, the dysulfiram/copper complex has demonstrated good safety profiles in some patients, although their medical effects require more verification. These progress has laid the foundation of clinical translation of copper-targeted remedies.

4. Cyrromatic effects between cuphoptosis and other cell death pathways

Cuproptosis displays crossstocks with other cell death mechanisms such as apoptosis and ferruptosis. For example, pkm2-dysulfiram/copper complexes simultaneously trigger cupoptosis and ferroptosis by preventing glycolitis and by promoting Fe-S cluster protein fall. Additionally, cuproptosis- induced immunogenic cell death (ICD) can increase Efficacy of Immune checkpoint inhibitor. These synergistic impact combinations provide new insight to develop treatments, although the accurate regulation of copper homostasis remains a challenge.

Future research instructions and challenges

As a newly identified mechanism of cellular demise, cuphoptosis is undergoing rigorous examination in various subjects, including chemotherapy, TME regulation, immune-based medical and result prediction, so that more effective cancer management strategies can be developed. However, the study of copoptosis is still a newborn area, in which the current study mainly focuses on its correlation with IBD and CRC. Additional fundamental examination requires, many underlying mechanisms are to be clarified. The future probe should focus on understanding accurate molecular routes that control cube metabolism and copoptosis in the context of IBD and CRC, as well as strategies to modify CU levels to maximize medical efficacy. Despite its ability, many challenges remain in the puroptosis research, which also gives rise to obstacles for clinical applications. First, potential clinical applications and safety concerns related to cuproptosis modulation are yet to be detected, which is facing important challenges for clinical translation of cuproptosis inducers. Copper deficiency and excess can induce both systemic toxicity, it requires additional clinical studies to evaluate how copper levels affect pregnancy in modulation IBD and CRC patients. Such investigations are important in improving targeting efficiency and in vivo stability of these therapeutic agents. Second, CU’s ability as a medical goal requires further exploration. This includes developing remedies based on CU metabolism and cuphoptosis, such as gene knockouts and cell-based approaches, while research attempts are transferred to novels copper indicators, including plant-rich compounds, synthetic molecules and nanotechnology-based carriers, which improve the affected cells. Additionally, the relationship between copper metabolism, copoptosis, and intestinal immune micro -generation requires further investigation. Combination of cuproptosis with immunotherapy IBD and CRC can provide a promising strategy to deal with, significantly improve the results of treatment and increase the patient’s survival. However, it is not clear whether the cuphoptosis and its signaling route play a protumer role in the initiation and development of the tumor. The current deficiency of valid cuproptosis biomarker underlines the need for additional research to enable accurate therapeutic interventions.

Understanding mutual action between alternative forms of cuproptosis and cellular demise forms another decisive research domain. Checking connections between copoptosis and other types of passages, including apoptosis, ferruptosis, and pyroptosis, can deepen our understanding of CU-related diseases and accelerates the progression of targeted remedies to induce tumor cell death more effectively. Further, the discovery of specific biomarckers and individual antitumor strategies will probably enable the clinical translation of treatments based on CU metabolism and cuphoptosis.

In summary, cuproptosis represents a potential novel medical avenue for IBD and CRC. Powering an understanding of cuproptosis regulation and enhancing its induction efficiency status as a novel therapeutic strategy for the intervention of the disease. This strategy not only has the ability to effectively suppress the onset and progress of the disease, but also to improve the patient’s survival and quality of life through accurate therapy. Therefore, understanding the involvement of copoptosis in pathological processes and developing related treatment strategies is sufficient scientific and medical importance.