An essential characteristic of quantum dots (QDs) is their antimicrobial activity. Compared with conventional antibiotics, QDs not only possess photoluminescence properties for imaging and photodynamic therapy but also have high structural stability. To enhance their antimicrobial efficiency, QDs usually are functionalized by polymers, including poly(ethylene glycol), polyethyleneimine, and poly-l-lysine. Also, QDs conjugated with polymers, such as poly(vinylpyrrolidone) and polyvinylidene fluoride, are prepared as antimicrobial membranes. The main antimicrobial mechanisms of QDs are associated with inducing free radicals, disrupting cell walls/membranes, and arresting gene expression. The different mechanisms from traditional antibiotics allow QDs to play antimicrobial roles in multi-drug-resistant bacteria and fungi. Since the toxicity of the QDs on animal cells is relatively low, they have broad application in antimicrobial research as an effective alternative of traditional antibiotics.

Carbon tetrachloride (CCl4)‐induced liver injury is predominantly caused by free radicals, in which mitochondrial function of hepatocytes is impaired, accompanying with the production of ROS and decreased ATP energy supply in animals intoxicated with CCl4. Here we explored a novel therapeutic approach, mitochondrial transplantation therapy, for treating the liver injury. The results showed that mitochondria entered hepatocytes through macropinocytosis pathway, and thereby cell viability was recovered in a concentration‐dependent manner. Mitochondrial therapy could increase ATP supply and reduce free radical damage. In liver injury model of mice, mitochondrial therapy significantly improved liver function and prevented tissue fibrogenesis. Transcriptomic data revealed that mitochondrial unfold protein response (UPRmt), a protective transcriptional response of mitochondria‐to‐nuclear retrograde signaling, would be triggered after mitochondrial administration. Then the anti‐oxidant genes were up‐regulated to scavenge free radicals. The mitochondrial function was rehabilitated through the transcriptional activation of respiratory chain enzyme and mitophage‐associated genes. The protective response re‐balanced the cellular homeostasis, and eventually enhanced stress resistance that is linked to cell survival. The efficacy of mitochondrial transplantation therapy in the animals would suggest a novel approach for treating liver injury caused by toxins.

Photodynamic theranostics/therapy (PDT) is a potential strategy for selectively imaging malignant sites and treating cancer via a non-invasive therapeutic method. Photosensitizers, the crucial components of PDT, enable colocalization of photons and light, and photon/light therapy in the therapeutic window of 400–900 nm exhibits photo­cyto­toxicity to tumor cells. Due to their high biostability and photo­cyto­toxicity, nano­photo­sensitizers (NPSs) are of much interest for malignant tumor theranostics at present. NPS-activated photons transfer energy through the absorption of a photon and convert molecular oxygen to the singlet reactive oxygen species, which leads to apoptosis and necrosis. Moreover, NPSs modified by polymers, including PLGA, PEG-PLA, PDLLA, PVCL-g-PLA, and P­(VCL-co-VIM)-g-PLA, exhibit excellent biocompatibility, and a tumor-targeting molecule linked on the nanoparticle surface can precisely deliver NPSs into the tumor region. The development of NPSs will accelerate the progress in tumor theranostics through the photon/light pathway.

In modern research, mitochondria are considered a more crucial energy plant in cells. Mitochondrial dysfunction, including mitochondrial DNA (mtDNA) mutation and denatured protein accumulation, is a common feature of tumors. The dysfunctional mitochondria reprogram molecular metabolism and allow tumor cells to proliferate in the hostile microenvironment. One of the crucial signaling pathways of the mitochondrial dysfunction activation in the tumor cells is the retrograde signaling of mitochondria-nucleus interaction, mitochondrial unfolded protein response (UPRmt), which is initiated by accumulation of denatured protein and excess ROS production. In the process of UPRmt, various components are activitated to enhance the mitochondria-nucleus retrograde signaling to promote carcinoma progression, including hypoxia-inducible factor (HIF), activating transcription factor ATF-4, ATF-5, CHOP, AKT, AMPK. The retrograde signaling molecules of overexpression ATF-5, SIRT3, CREB, SOD1, SOD2, early growth response protein 1 (EGR1), ATF2, CCAAT/enhancer-binding protein-d, and CHOP also involved in the process. Targeted blockage of the UPRmt pathway could obviously inhibit tumor proliferation and metastasis. This review indicates the UPRmt pathways and its crucial role in targeted therapy of metastasis tumors.

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