Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Ver. Summary Created by Modification Content Size Created at Operation
1 -- 2536 2022-11-08 10:18:32 |
2 format correct + 4 word(s) 2540 2022-11-09 08:37:15 |

Video Upload Options

Do you have a full video?


Are you sure to Delete?
If you have any further questions, please contact Encyclopedia Editorial Office.
Liu, W.;  Ma, X.;  Kheyr, S.M.;  Dong, A.;  Zhang, J. Functionalization Strategies of Nanocarriers. Encyclopedia. Available online: (accessed on 08 December 2023).
Liu W,  Ma X,  Kheyr SM,  Dong A,  Zhang J. Functionalization Strategies of Nanocarriers. Encyclopedia. Available at: Accessed December 08, 2023.
Liu, Weiming, Xinyu Ma, Shuayb Mohamed Kheyr, Anjie Dong, Jianhua Zhang. "Functionalization Strategies of Nanocarriers" Encyclopedia, (accessed December 08, 2023).
Liu, W.,  Ma, X.,  Kheyr, S.M.,  Dong, A., & Zhang, J.(2022, November 08). Functionalization Strategies of Nanocarriers. In Encyclopedia.
Liu, Weiming, et al. "Functionalization Strategies of Nanocarriers." Encyclopedia. Web. 08 November, 2022.
Functionalization Strategies of Nanocarriers

The applications of nanoparticles (NPs) for drug delivery have achieved great achievements and shown enormous advantages. However, the efficient delivery of chemotherapeutic drugs to target cells was still severely restricted by various anatomical and physiological barriers. Consequently, the NPs were designed and functionalized in order to achieve active and specific targeting for promoting the preferential accumulation in tumor tissues, effective uptake by tumor cells, and release of the drug after entering cancer cells.

covalent organic frameworks nanocarriers drug delivery

1. Passive Targeting Strategies

The unique tumor microenvironment (TME) and the pathophysiological characteristics of tumor tissues are one of the main barriers to drug delivery [1][2]. However, the physicochemical characteristics and unique nanostructures of nanoparticles (NPs) can be preferably accumulated at the tumor site by the enhanced permeability and retention (EPR) effect [3]. The preferential accumulation of NPs in tumors is because solid tumors usually possess several pathophysiological characteristics: the hyper vascularization and secretion of vascular permeability factors that allow NPs to translocate from the blood compartment to the perivascular TME, and thus cause enhanced permeation t [4]. Other pathophysiological characteristics of solid tumors are their abnormal form, characterized by fenestrations, the rough muscle layer, and the absence of effective intratumor lymphatic drainage. When the drug-loaded NPs are extravasated into the interstitial space of the tumor, the NPs’ diffusion back into the bloodstream is usually prevented, as their flow rate to the exterior bloodstream of the tumor is slowed down due to the dense collagen matrix. Thus, the drug-loaded NPs are retained in the interstitium for a longer time, leading to effective targeting of the tumor [5], wherein the drug is released through enzymatic degradation and internalized by the cells through passive diffusion [6]. A nanosystem size between 10 and 200 nm is suitable for an efficient and non-damaging treatment since NPs with sizes of over 200 nm can be easily trapped by the liver and spleen, which belong to the reticuloendothelial system (RES) and are often associated with the mononuclear phagocyte system (MPS). In the same way, NPs with a size below 8 nm are quickly cleared by renal filtration [7]. However, size is not the only factor that influences the EPR effect, but also the shape of the NPs plays an important role in the diffusion throughout the tumor tissue. For example, some nanorods have exhibited more rapid tumor penetration than nanospheres [8][9], thus enhancing tumor penetration and accumulation.
Tumor heterogeneity and intrinsic features of TME, such as hypoxic gradient, acidosis, high interstitial fluid pressure, and low microvascular pressure, can limit the delivery of nanomedical drugs to the tumor by passive targeting, thus affecting their efficacy [10]. In addition, the delivery efficiency and the resultant therapeutic efficacy are obviously determined by the blood circulation time of NPs. After entering the human body, NPs inevitably contact a huge variety of biomolecules, such as sugars, proteins, and lipids. The nano-bio interactions lead to the formation of the so-called “protein corona” on the outer surfaces of NPs [11]. The transport behavior of NPs in blood and the clearance by the reticuloendothelial system and/or mononuclear phagocytic system are dictated by the physicochemical properties of NPs, such as particle size, particle shape, and surface feature [12]. To achieve good dispersion in serum, NPs are mostly coated with biosafe surfactants, hydrophilic polymers, and biodegradable copolymers, especially polyethylene glycol (PEG). The surface conjugation of PEG can significantly suppress the interactions between NPs with blood components, such as plasma proteins and enzymes. As a result, the circulation time of NPs are prolonged significantly and thus improve the EPR effect and enhance therapeutic results [5]. Despite the great success of PEG-conjugated substances, an unexpected immunogenic response of PEG (accelerated blood clearance phenomenon) has been extensively observed during the repeated administration of PEGylated nanocarriers, leading to increased clearance. Recently, cell membrane biomimetic NPs were widely designed and some special functions were realized, such as the prolonged blood circulation time, immune escape, and specific recognition. Generally, the human serum albumin or red blood cell membrane, as well as the macrophage plasma membrane, were extracted from leukocytes, red blood cells, and macrophage plasma, which were used as “self-markers” to coat onto the outer surface of various NPs. The biomimetic NPs can inherit the unique biofunction of the cell membrane to prevent recognition and clearance [13][14].

2. Active Targeting Strategies

The past several decades have witnessed great progress in passive nanoparticle targeting strategies. As an important concept in nanomedicine, some passively targeted NPs, for example, long-circulating liposomes, have been approved by FDA for the treatment of solid tumors. However, the passive targeting strategies just via the EPR effect cannot ensure complete targeted delivery. Due to the complex biological barriers within the body, some studies have confirmed that most of the administered NPs were found to be captured and removed by mononuclear phagocyte systems, thus ending up in non-target sites. A recent analysis reported that only about 1% of the injected NPs dose reaches the tumor. Most of the administered NPs were found in healthy organs such as the liver and spleen. The amount of NPs accumulated within the targeted tumor is insufficient to induce an antitumor response [15]. In contrast to passive targeting strategies, active targeting NPs with specific surface ligands can recognize and bind to specific cell surface receptors on cancerous cells [16][17]. The active targeting ligands, including peptides, proteins, nucleic acids, aptamers, sugars, and small molecules such as folic acid and carbohydrates have been widely used to functionalize NPs [18]. The ligand-modified NPs can increase the specific interaction with targeted diseased cells [19]. As a result, this kind of strategy can improve the affinities of NPs to tumor cells, increase the retention of NPs at diseased sites, and promote the uptake of NPs by cancer cells, leading to a significant improvement in the delivery efficacy and an obvious decrease in the toxicity of therapeutic agents. For example, folate is a vitamin with a high affinity for the folic acid receptor, overexpressed in the TME and certain tumors from 100 to 300 times above endogenous levels, so several folate-modified strategies have been widely developed by the synthesis of folic acid–drug conjugates or the grafting of folic acid onto the outer surface of nanocarriers. In addition to the active targeting of receptor overexpressed in tumor cells or tumor tissues, the tumor vasculature is a viable drug target. The tumor vasculature is not simply blood vessels. Compared with normal vasculature, tumor vasculature generally has a disorganized structure, abnormal cell adhesions, and basement membrane structures, as well as an especially inefficient blood supply. Clearly, the tumor vasculature is significantly different from the normal vessels. Therefore, the active targeting of the tumor vasculature, generally on the basis of the positive and negative regulation of angiogenesis/lymphangiogenesis, has been widely used as a novel strategy to enhance the accumulation of drug-loaded NPs into tumors, especially in combination with antitumor therapy along with anti-angiogenic therapies [20]. In addition to the current extracellular targeting strategies as mentioned above, the intracellular targeting strategies, especially the nuclear targeting strategy, can also increase the therapeutic efficacy by minimizing off-target effects. This kind of targeting strategy is dependent on specific peptide signals, which can interact with organelle receptors such as the nucleus, mitochondrion, and peroxisome through passive diffusion and active transport, allowing for the controlled release of the payload in the appropriate subcellular location [21]. The properties of the ligands concerning size, density, orientation, charge, and affinity must be taken into account [22]. Since NPs’ avidity is directly related to ligand density, achieving high ligand surface density and low nanocarrier opsonization is the main goal not only to attain high targeting efficiency but also to increase cell binding, and ensure optimal internalization and improve drug accumulation in tumors when studied in vivo [23]. Furthermore, the phenomenon called the “binding site barrier” at the tumor periphery is crucial to create ligand–receptor interactions strong enough to reach the targeting sites but without hampering the penetration of functionalized nanocarriers into the interstitial space [20]. Hence, the binding of the appropriate ligands on the NPs surface is of essential importance for designing active target systems. Strategies for ligand attachment are based on either covalent bonding or physical adsorption using affinity complexes. In the former, the ligands, mainly small molecules, are either bound to the NPs before assembly (pre-formulation strategy), or they can also be bound by reacting with formulated NPs (post-formulation conjugation), involving all types of ligands, preferably those that are not stable in organic solvents, have a large size, or have physicochemical properties that are not compatible with copolymers. In addition, “click chemistry” could be a useful synthetic method for conjugation, which involves a one-step reaction of heteroatom bonds with or without catalysts.
Despite the growing potential of nanomedicine in the field of site-specific delivery based on various targeting strategies, brain-targeted drug delivery still presents a tremendous challenge to scientists, as the existence of the blood–brain barrier (BBB) can dramatically impede the systemic delivery of pharmaceuticals from the blood into the brain. Intensive research has been devoted to developing promising and attractive strategies to enable nanomedicines or therapeutics effectively circumvent BBB. Active targeting by the surface modification of NPs with specific ligands that can be recognized by transporters (glucose, glutathione, and amino acids transporters) or receptors (transferrin, lactoferrin, LDL, nAChR, and αvβ3 integrin receptors) overexpressed in the brain has been widely used to direct NPs to the desired site of action in the brain. Unfortunately, although there are some undergoing clinical trials, so far, most nanomedicines have not exhibited a significant improvement in therapy efficacy for brain tumors, and thus no nanoformulations have received approval for clinical use. Therefore, there is an urgent need for strategies to develop more advanced multifunctional nanomedicines, which can increase the survival rate of brain tumor patients [24].

3. Stimuli-Responsive Strategies

As one of the latest advances in nanomedicine, stimuli-responsive systems, also known as smart systems, represent a major advance in the design of nanomaterials capable of gradually releasing their payload, keeping low therapeutic levels of the drug during blood circulation but boosting them when NPs reach targeting sites, after which these levels are maintained.
Controlled release strategies lead to the development of smart drug delivery systems. This kind of smart system can not only change their structure, morphology, size, and stability, as well as surface properties in response to internal/external stimuli, but can also overcome biological barriers by the reemergence of active targeting ligands via shielding/deshielding transition. As a result, these responsive nanocarriers can activate the drug release at the site of targeted tumors, leading to lower drug toxicity and thus better therapeutic efficiency [25][26][27]. The main structure in smart nanoplatforms is usually stimuli-responsive polymers that are found as linkers forming part of the skeleton, as polymer conjugates on the outer surface of the nanocarrier, or as polymer–drug conjugates binding bioactive molecules to the nanocarrier [4].
Some different stimuli have been used for controlling drug delivery on the basis of internal and external stimuli. The internal stimuli-responsive nanocarriers can undergo transitions in response to endogenous characteristics or biomarkers such as changes in pH, redox potential, and enzymes, as well as temperature. On the contrary, the external stimuli-sensitive nanocarriers can take advantage of exogenous variables such as light and ultrasound [28][29][30][31]. The internal stimulus-sensitive nanocarriers can provide a relatively universal approach not only for controlled drug release but also for prodrug activation and endosome/lysosome escape [32][33]. The cancer microenvironment is characterized by acidosis and hypoxia due to the presence of lactate; thus, there is a difference between intracellular (6.5–6.8) and extracellular (7.4) pH in cancer cells [28]. The design of the NPs targeted at this mildly acidic TME with the ability to differentiate small pH variations for subsequent delivery of weak basic agents or anticancer drugs, e.g., doxorubicin, improves their accumulation in acidic fluids, and increases the intercellular uptake of drugs and adjusts the drug release within tumor cells from the nanocarriers [5][30][31][34]. In addition to pH-sensitive nanocarriers, hypoxia-sensitive nanocarriers could also be employed, as solid tumors show decreased oxygen levels around them and decrease the effectiveness of a wide range of cancer therapies [35][36]. These nanocarriers are generally made of hypoxia-sensitive materials or their derivatives and are designed to increase the oxygen level of TME through the release of hypoxia-activated prodrugs [37][38].
Abnormal redox balance is one of the characteristics of TME. Glutathione (GSH) is a natural antioxidant whose levels within cancer cells (2–10 mM) are significantly higher than those in healthy cells (2–10 μM) [39], so it can be used as an endogenous trigger for cancer treatments by developing redox-responsive nanomaterials for drug delivery. The latter approach could be applied mainly in combination therapies, as GSH helps modulate and prevent the damage caused by toxic reactive oxygen species (ROS), so the development of GSH-responsive nanoplatforms is necessary to trigger both the generation of ROS and the release of ROS-responsive drugs, thus enabling the disruption of redox self-regulation in cancer cells and an improved therapeutic effect. Disulfide- and diselenide-containing materials are more widely used because of their lower bounding energies and high sensitivity to redox potential [40]. Temperature, light, ultrasound, or magnetic field as typical external stimuli have been widely used to design smart NPs for improved delivery efficacy, which makes it possible to control the location, intensity, and duration of exogenous stimuli so that triggering a controlled release of the payload [41][42][43].
Due to the complicated physiological fluids, complex physiopathological mechanisms, and the high heterogeneity of tumor tissues as well as the abnormal TME, the single stimulus-responsive drug-delivery system often cannot overcome the sequential biological barriers and cannot meet the requirements of complex clinical applications. In the last several decades, there has been a trend to incorporate multiple stimuli to trigger drug release for efficient drug delivery. The multi-modal nanocarriers can take advantage of a mixture of endogenous/exogenous stimuli or can combine diagnostic and therapeutic functionalities into a single nanoplatform. This strategy can not only facilitate NPs to overcome a series of continuous physiopathological barriers in the body, but can also achieve cancer therapies and cancer imaging simultaneously [29][44][45][46][47].
Although many achievements have been made in the development of NP-based chemotherapies, the performance of various NPs is still far from perfect. There are still many challenges that must be addressed to overcome the complex biological barriers and enhance the delivery efficiency of nanomedicine. For example, most traditional nanocarriers, especially liposomes, polymer micelles, and polymer nanogels, always suffer from their low drug loading capacity. The low drug loading content often leads to poor treatment efficacy. In this case, an increase in dosage and/or frequency of administration is required to deliver enough drugs at the specific sites. In addition, these nanocarriers often suffer from an uncontrollable release profile, especially premature drug leakage. Apparently, the premature drug leakage outside the tumor tissue not only causes local or systemic toxicity, but also decreases the bioavailability of nanomedicines and thus restricts the therapeutic efficacy [48][49]. In addition to the undesirable initial burst release, the delayed or inferior drug release within the tumor cells would inevitably cause a very low therapeutic efficacy of nanomedicines, as tumor cells possess an active efflux mechanism and intrinsic drug resistance mechanism to remove intracellular drugs. In addition, the inorganic or metal NPs have exhibited great potential for pharmaceutical applications. However, their applications often suffer from relatively low biocompatibility and relatively high toxicity as well as undesired biodegradation behaviors, limiting clinical translation. Apparently, it is imperative to develop novel and more sophisticated nanocarriers for effective cancer treatment.


  1. Kim, M.; Lee, J.; Nam, J. Plasmonic Photothermal Nanoparticles for Biomedical Applications. Adv. Sci. 2019, 6, 1900471.
  2. Ji, T.; Zhao, Y.; Ding, Y.; Nie, G. Using Functional Nanomaterials to Target and Regulate the Tumor Microenvironment: Diagnostic and Therapeutic Applications. Adv. Mater. 2013, 25, 3508–3525.
  3. Nichols, J.W.; Bae, Y.H. Odyssey of a Cancer Nanoparticle: From Injection Site to Site of Action. Nano Today 2012, 7, 606–618.
  4. Alasvand, N.; Urbanska, A.M.; Rahmati, M.; Saeidifar, M.; Gungor-Ozkerim, P.S.; Sefat, F.; Rajadas, J.; Mozafari, M. Chapter 13—Therapeutic Nanoparticles for Targeted Delivery of Anticancer Drugs. Multifunct. Syst. Comb. Deliv. Biosensing Diagn. 2017, 2017, 245–259.
  5. Wibroe, P.P.; Ahmadvand, D.; Oghabian, M.A.; Yaghmur, A.; Moghimi, S.M. An Integrated Assessment of Morphology, Size, and Complement Activation of the PEGylated Liposomal Doxorubicin Products Doxil®, Caelyx®, DOXOrubicin, and SinaDoxosome. J. Control. Release 2016, 221, 1–8.
  6. Wang, L.; Huo, M.; Chen, Y.; Shi, J. Tumor Microenvironment-Enabled Nanotherapy. Adv. Healthc. Mater. 2018, 7, 1701156.
  7. Deng, H.; Song, K.; Zhang, J.; Deng, L.; Dong, A.; Qin, Z. Modulating the Rigidity of Nanoparticles for Tumor Penetration. Chem. Commun. 2018, 54, 3014–3017.
  8. Blanco, E.; Hsiao, A.; Mann, A.P.; Landry, M.G.; Meric-Bernstam, F.; Ferrari, M. Nanomedicine in Cancer Therapy: Innovative Trends and Prospects. Cancer Sci. 2011, 102, 1247–1252.
  9. Gerlowski, L.E.; Jain, R.K. Microvascular Permeability of Normal and Neoplastic Tissues. Microvasc. Res. 1986, 31, 288–305.
  10. Sykes, E.A.; Chen, J.; Zheng, G.; Chan, W.C.W. Investigating the Impact of Nanoparticle Size on Active and Passive Tumor Targeting Efficiency. ACS Nano 2014, 8, 5696–5706.
  11. Gullotti, E.; Yeo, Y. Extracellularly Activated Nanocarriers: A New Paradigm of Tumor Targeted Drug Delivery. Mol. Pharm. 2009, 6, 1041–1051.
  12. von Roemeling, C.; Jiang, W.; Chan, C.K.; Weissman, I.L.; Kim, B.Y.S. Breaking Down the Barriers to Precision Cancer Nanomedicine. Trends Biotechnol. 2017, 35, 159–171.
  13. Rodriguez, P.L.; Harada, T.; Christian, D.A.; Pantano, D.A.; Tsai, R.K.; Discher, D.E. Minimal “Self” Peptides That Inhibit Phagocytic Clearance and Enhance Delivery of Nanoparticles. Science 2013, 339, 971–975.
  14. Hu, C.-M.J.; Zhang, L.; Aryal, S.; Cheung, C.; Fang, R.H.; Zhang, L. Erythrocyte Membrane-Camouflaged Polymeric Nanoparticles as a Biomimetic Delivery Platform. Proc. Natl. Acad. Sci. USA 2011, 108, 10980–10985.
  15. Attia, M.F.; Anton, N.; Wallyn, J.; Omran, Z.; Vandamme, T.F. An Overview of Active and Passive Targeting Strategies to Improve the Nanocarriers Efficiency to Tumour Sites. J. Pharm. Pharmacol. 2019, 71, 1185–1198.
  16. Kamaly, N.; Xiao, Z.; Valencia, P.M.; Radovic-Moreno, A.F.; Farokhzad, O.C. Targeted Polymeric Therapeutic Nanoparticles: Design, Development and Clinical Translation. Chem. Soc. Rev. 2012, 41, 2971.
  17. Wang, X.; Li, S.; Shi, Y.; Chuan, X.; Li, J.; Zhong, T.; Zhang, H.; Dai, W.; He, B.; Zhang, Q. The Development of Site-Specific Drug Delivery Nanocarriers Based on Receptor Mediation. J. Control. Release 2014, 193, 139–153.
  18. Panyam, J.; Zhou, W.; Prabha, S.; Sahoo, S.K.; Labhasetwar, V. Rapid Endo-lysosomal Escape of Poly(DL-lactide- Co Glycolide) Nanoparticles: Implications for Drug and Gene Delivery. FASEB J. 2002, 16, 1217–1226.
  19. Saha, R.N.; Vasanthakumar, S.; Bende, G.; Snehalatha, M. Nanoparticulate Drug Delivery Systems for Cancer Chemotherapy. Mol. Membr. Biol. 2010, 27, 215–231.
  20. Chen, D.; Qu, X.; Shao, J.; Wang, W.; Dong, X. Anti-Vascular Nano Agents: A Promising Approach for Cancer Treatment. J. Mater. Chem. B 2020, 8, 2990–3004.
  21. Liang, P.; Huang, X.; Wang, Y.; Chen, D.; Ou, C.; Zhang, Q.; Shao, J.; Huang, W.; Dong, X. Tumor-Microenvironment-Responsive Nanoconjugate for Synergistic Antivascular Activity and Phototherapy. ACS Nano 2018, 12, 11446–11457.
  22. Bertrand, N.; Wu, J.; Xu, X.; Kamaly, N.; Farokhzad, O.C. Cancer nanotechnology: The impact of passive and active targeting in the era of modern cancer biology. Adv. Drug Deliv. Rev. 2014, 66, 2–25.
  23. Li, Z.; Song, N.; Yang, Y.-W. Stimuli-Responsive Drug-Delivery Systems Based on Supramolecular Nanovalves. Matter 2019, 1, 345–368.
  24. Khan, A.R.; Yang, X.; Fu, M.; Zhai, G. Recent progress of drug nanoformulations targeting to brain. J. Control. Release 2018, 291, 37–64.
  25. Luo, F.; Fan, Z.; Yin, W.; Yang, L.; Li, T.; Zhong, L.; Li, Y.; Wang, S.; Yan, J.; Hou, Z.; et al. PH-Responsive Stearic Acid-O-Carboxymethyl Chitosan Assemblies as Carriers Delivering Small Molecular Drug for Chemotherapy. Mater. Sci. Eng. C 2019, 105, 110107.
  26. de Bree, E.; Romanos, J.; Tsiftsis, D.D. Hyperthermia in Anticancer Treatment. Eur. J. Surg. Onc. 2002, 28, 95.
  27. Holme, M.N.; Fedotenko, I.A.; Abegg, D.; Althaus, J.; Babel, L.; Favarger, F.; Reiter, R.; Tanasescu, R.; Zaffalon, P.-L.; Ziegler, A.; et al. Shear-Stress Sensitive Lenticular Vesicles for Targeted Drug Delivery. Nat. Nanotechnol. 2012, 7, 536–543.
  28. Lee, E.S.; Gao, Z.; Bae, Y.H. Recent Progress in Tumor PH Targeting Nanotechnology. J. Control. Release 2008, 132, 164–170.
  29. Zhou, M.; Wei, W.; Chen, X.; Xu, X.; Zhang, X.; Zhang, X. PH and Redox Dual Responsive Carrier-Free Anticancer Drug Nanoparticles for Targeted Delivery and Synergistic Therapy. Nanomedicine 2019, 20, 102008.
  30. Meng, F.; Zhong, Y.; Cheng, R.; Deng, C.; Zhong, Z. PH-Sensitive Polymeric Nanoparticles for Tumor-Targeting Doxorubicin Delivery: Concept and Recent Advances. Nanomedicine 2014, 9, 487–499.
  31. Deng, H.; Liu, J.; Zhao, X.; Zhang, Y.; Liu, J.; Xu, S.; Deng, L.; Dong, A.; Zhang, J. PEG- b -PCL Copolymer Micelles with the Ability of PH-Controlled Negative-to-Positive Charge Reversal for Intracellular Delivery of Doxorubicin. Biomacromolecules 2014, 15, 4281–4292.
  32. Chen, F.; Cai, W. Nanomedicine for Targeted Photothermal Cancer Therapy: Where Are We Now? Nanomedicine 2015, 10, 1–3.
  33. Mi, P. Stimuli-Responsive Nanocarriers for Drug Delivery, Tumor Imaging, Therapy and Theranostics. Theranostics 2020, 10, 4557–4588.
  34. Hashemzadeh, H.; Raissi, H. Understanding Loading, Diffusion and Releasing of Doxorubicin and Paclitaxel Dual Delivery in Graphene and Graphene Oxide Carriers as Highly Efficient Drug Delivery Systems. Appl. Surf. Sci. 2020, 500, 144220.
  35. Kwon, S.; Ko, H.; You, D.G.; Kataoka, K.; Park, J.H. Nanomedicines for Reactive Oxygen Species Mediated Approach: An Emerging Paradigm for Cancer Treatment. Acc. Chem. Res. 2019, 52, 1771–1782.
  36. Chen, D.; Wang, Z.; Dai, H.; Lv, X.; Ma, Q.; Yang, D.; Shao, J.; Xu, Z.; Dong, X. Boosting O 2 •− Photogeneration via Promoting Intersystem-Crossing and Electron-Donating Efficiency of Aza-BODIPY-Based Nanoplatforms for Hypoxic-Tumor Photodynamic Therapy. Small Methods 2020, 4, 2000013.
  37. Yang, B.; Chen, Y.; Shi, J. Reactive Oxygen Species (ROS)-Based Nanomedicine. Chem. Rev. 2019, 119, 4881–4985.
  38. Yu, S.; Chen, Z.; Zeng, X.; Chen, X.; Gu, Z. Advances in Nanomedicine for Cancer Starvation Therapy. Theranostics 2019, 9, 8026–8047.
  39. Trachootham, D.; Alexandre, J.; Huang, P. Targeting Cancer Cells by ROS-Mediated Mechanisms: A Radical Therapeutic Approach? Nat. Rev. Drug Discov. 2009, 8, 579–591.
  40. Chen, Q.; Xu, L.; Liang, C.; Wang, C.; Peng, R.; Liu, Z. Photothermal Therapy with Immune-Adjuvant Nanoparticles Together with Checkpoint Blockade for Effective Cancer Immunotherapy. Nat. Commun. 2016, 7, 13193.
  41. Zhou, Z.; Song, J.; Nie, L.; Chen, X. Reactive Oxygen Species Generating Systems Meeting Challenges of Photodynamic Cancer Therapy. Chem. Soc. Rev. 2016, 45, 6597–6626.
  42. Nosaka, Y.; Nosaka, A.Y. Generation and Detection of Reactive Oxygen Species in Photocatalysis. Chem. Rev. 2017, 117, 11302–11336.
  43. Agostinis, P.; Berg, K.; Cengel, K.A.; Foster, T.H.; Girotti, A.W.; Gollnick, S.O.; Hahn, S.M.; Hamblin, M.R.; Juzeniene, A.; Kessel, D.; et al. Photodynamic Therapy of Cancer: An Update. CA Cancer J. Clin. 2011, 61, 250–281.
  44. Wang, Y.; Zhou, K.; Huang, G.; Hensley, C.; Huang, X.; Ma, X.; Zhao, T.; Sumer, B.D.; DeBerardinis, R.J.; Gao, J. A Nanoparticle-Based Strategy for the Imaging of a Broad Range of Tumours by Nonlinear Amplification of Microenvironment Signals. Nat. Mater. 2014, 13, 204–212.
  45. Liong, M.; Lu, J.; Kovochich, M.; Xia, T.; Ruehm, S.G.; Nel, A.E.; Tamanoi, F.; Zink, J.I. Multifunctional Inorganic Nanoparticles for Imaging, Targeting, and Drug Delivery. ACS Nano 2008, 2, 889–896.
  46. Lin, J.; Li, Y.; Li, Y.; Wu, H.; Yu, F.; Zhou, S.; Xie, L.; Luo, F.; Lin, C.; Hou, Z. Drug/Dye-Loaded, Multifunctional PEG–Chitosan–Iron Oxide Nanocomposites for Methotraxate Synergistically Self-Targeted Cancer Therapy and Dual Model Imaging. ACS Appl. Mater. Inter. 2015, 7, 11908–11920.
  47. Dong, Z.; Gong, H.; Gao, M.; Zhu, W.; Sun, X.; Feng, L.; Fu, T.; Li, Y.; Liu, Z. Polydopamine Nanoparticles as a Versatile Molecular Loading Platform to Enable Imaging-Guided Cancer Combination Therapy. Theranostics 2016, 6, 1031–1042.
  48. Chen, H.; Zhang, W.; Zhu, G.; Xie, J.; Chen, X. Rethinking Cancer Nanotheranostics. Nat. Rev. Mater. 2017, 2, 17024.
  49. Sun, Q.; Radosz, M.; Shen, Y. Challenges in Design of Translational Nanocarriers. J. Control. Release 2012, 164, 156–169.
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to : , , , ,
View Times: 198
Revisions: 2 times (View History)
Update Date: 09 Nov 2022