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      Electrospun Fibers Control Drug Delivery for Tissue Regeneration and Cancer Therapy

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          Abstract

          Versatile strategies have been developed to construct electrospun fiber-based drug delivery systems for tissue regeneration and cancer therapy. We first introduce the construction of electrospun fiber scaffolds and their various structures, as well as various commonly used types of drugs. Then, we discuss some representative strategies for controlling drug delivery by electrospun fibers, with specific emphasis on the design of endogenous and external stimuli-responsive drug delivery systems. Afterwards, we summarize the recent progress on controlling drug delivery with electrospun fiber scaffolds for tissue engineering, including soft tissue engineering (such as skin, nerve, and cardiac repair) and hard tissue engineering (such as bone, cartilage, and musculoskeletal systems), as well as for cancer therapy. Furthermore, we provide future development directions and challenges facing the use of electrospun fibers for controlled drug delivery, aiming to provide insights and perspectives for the development of smart drug delivery platforms and improve clinical therapeutic effects in tissue regeneration and cancer therapy.

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          Electrospinning and Electrospun Nanofibers: Methods, Materials, and Applications

          Jiajia Xue, Tong Wu, Yunqian Dai … (2019)
          Electrospinning is a versatile and viable technique for generating ultrathin fibers. Remarkable progress has been made with regard to the development of electrospinning methods and engineering of electrospun nanofibers to suit or enable various applications. We aim to provide a comprehensive overview of electrospinning, including the principle, methods, materials, and applications. We begin with a brief introduction to the early history of electrospinning, followed by discussion of its principle and typical apparatus. We then discuss its renaissance over the past two decades as a powerful technology for the production of nanofibers with diversified compositions, structures, and properties. Afterward, we discuss the applications of electrospun nanofibers, including their use as “smart” mats, filtration membranes, catalytic supports, energy harvesting/conversion/storage components, and photonic and electronic devices, as well as biomedical scaffolds. We highlight the most relevant and recent advances related to the applications of electrospun nanofibers by focusing on the most representative examples. We also offer perspectives on the challenges, opportunities, and new directions for future development. At the end, we discuss approaches to the scale-up production of electrospun nanofibers and briefly discuss various types of commercial products based on electrospun nanofibers that have found widespread use in our everyday life.
          Article 0 comments Cited 976 times – based on 0 reviews     Review now
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            Parkinson's disease

            Bastiaan Bloem, Michael Okun, Christine Klein (2021)
            Parkinson's disease is a recognisable clinical syndrome with a range of causes and clinical presentations. Parkinson's disease represents a fast-growing neurodegenerative condition; the rising prevalence worldwide resembles the many characteristics typically observed during a pandemic, except for an infectious cause. In most populations, 3-5% of Parkinson's disease is explained by genetic causes linked to known Parkinson's disease genes, thus representing monogenic Parkinson's disease, whereas 90 genetic risk variants collectively explain 16-36% of the heritable risk of non-monogenic Parkinson's disease. Additional causal associations include having a relative with Parkinson's disease or tremor, constipation, and being a non-smoker, each at least doubling the risk of Parkinson's disease. The diagnosis is clinically based; ancillary testing is reserved for people with an atypical presentation. Current criteria define Parkinson's disease as the presence of bradykinesia combined with either rest tremor, rigidity, or both. However, the clinical presentation is multifaceted and includes many non-motor symptoms. Prognostic counselling is guided by awareness of disease subtypes. Clinically manifest Parkinson's disease is preceded by a potentially long prodromal period. Presently, establishment of prodromal symptoms has no clinical implications other than symptom suppression, although recognition of prodromal parkinsonism will probably have consequences when disease-modifying treatments become available. Treatment goals vary from person to person, emphasising the need for personalised management. There is no reason to postpone symptomatic treatment in people developing disability due to Parkinson's disease. Levodopa is the most common medication used as first-line therapy. Optimal management should start at diagnosis and requires a multidisciplinary team approach, including a growing repertoire of non-pharmacological interventions. At present, no therapy can slow down or arrest the progression of Parkinson's disease, but informed by new insights in genetic causes and mechanisms of neuronal death, several promising strategies are being tested for disease-modifying potential. With the perspective of people with Parkinson's disease as a so-called red thread throughout this Seminar, we will show how personalised management of Parkinson's disease can be optimised.
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              The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis.

              Sumanth D. Prabhu, Nikolaos G. Frangogiannis (2016)
              In adult mammals, massive sudden loss of cardiomyocytes after infarction overwhelms the limited regenerative capacity of the myocardium, resulting in the formation of a collagen-based scar. Necrotic cells release danger signals, activating innate immune pathways and triggering an intense inflammatory response. Stimulation of toll-like receptor signaling and complement activation induces expression of proinflammatory cytokines (such as interleukin-1 and tumor necrosis factor-α) and chemokines (such as monocyte chemoattractant protein-1/ chemokine (C-C motif) ligand 2 [CCL2]). Inflammatory signals promote adhesive interactions between leukocytes and endothelial cells, leading to extravasation of neutrophils and monocytes. As infiltrating leukocytes clear the infarct from dead cells, mediators repressing inflammation are released, and anti-inflammatory mononuclear cell subsets predominate. Suppression of the inflammatory response is associated with activation of reparative cells. Fibroblasts proliferate, undergo myofibroblast transdifferentiation, and deposit large amounts of extracellular matrix proteins maintaining the structural integrity of the infarcted ventricle. The renin-angiotensin-aldosterone system and members of the transforming growth factor-β family play an important role in activation of infarct myofibroblasts. Maturation of the scar follows, as a network of cross-linked collagenous matrix is formed and granulation tissue cells become apoptotic. This review discusses the cellular effectors and molecular signals regulating the inflammatory and reparative response after myocardial infarction. Dysregulation of immune pathways, impaired suppression of postinfarction inflammation, perturbed spatial containment of the inflammatory response, and overactive fibrosis may cause adverse remodeling in patients with infarction contributing to the pathogenesis of heart failure. Therapeutic modulation of the inflammatory and reparative response may hold promise for the prevention of postinfarction heart failure.
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                Author and article information

                Contributors
                Journal
                Title: Advanced Fiber Materials
                Abbreviated Title: Adv. Fiber Mater.
                Publisher: Springer Science and Business Media LLC
                ISSN (Print): 2524-7921
                ISSN (Electronic): 2524-793X
                Publication date Created: December 2022
                Publication date (Electronic): September 16 2022
                Publication date (Print): December 2022
                Volume: 4
                Issue: 6
                Pages: 1375-1413
                Article
                DOI: 10.1007/s42765-022-00198-9
                SO-VID: ab192dde-0195-4bef-b8c4-4cfef67d63eb
                Copyright © © 2022
                License:

                https://creativecommons.org/licenses/by/4.0

                https://creativecommons.org/licenses/by/4.0

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