Current Drug Targets - Volume 23, Issue 16, 2022

The discovery of the roles of RNA other than just as a messenger, such as a ribozyme, and regulatory RNAs, such as microRNA and long noncoding RNAs, is fascinating. RNA is now recognized as an important regulator involved in practically every biological process. Research in the field of non-coding RNAs, specifically microRNAs (miRNAs) and long non-coding RNAs (LncRNAs) have developed immensely over the years. Recent studies identified diverse RNAs, including non-coding RNAs such as LncRNA and their various modes of action in the cells. These RNAs are anticipated to be key targets for the treatment of various diseases since they control a broad array of biological pathways. LncRNA-targeted drug platform delivers the pharmaceutical industry a myriad of opportunities and has the potential to modulate diseases at the genetic level while also overcoming the limitations of inconsistent proteins. This article focuses on the recent advancement as well as the major challenges in the field and describes the various RNA-based therapeutics that alter the quality of healthcare for many diseases and bring personalized medicines to fruition. The article also summarizes RNA-based therapeutics that are undergoing testing in clinical trials or have been granted FDA approval.

Now-a-days fungal infection emerges as a significant problem to healthcare management systems due to high frequency of associated morbidity, mortality toxicity, drug-drug interactions, and resistance of the antifungal agents. Aspergillus is the most common mold that cause infection in immunocompromised hosts. It's a hyaline mold that is cosmopolitan and ubiquitous in nature. Aspergillus infects around 10 million population each year with a mortality rate of 30-90%. Clinically available antifungal formulations are restricted to four classes (i.e., polyene, triazole, echinocandin, and allylamine), and each of them have their own limitations associated with the activity spectrum, the emergence of resistance, and toxicity. Consequently, novel antifungal agents with modified and altered chemical structures are required to combat these invasive fungal infections. To overcome these limitations, there is an urgent need for new antifungal agents that can act as potent drugs in near future. Currently, some compounds have shown effective antifungal activity. In this review article, we have discussed all potential antifungal therapies that contain old antifungal drugs, combination therapies, and recent novel antifungal formulations, with a focus on the Aspergillus associated infections.

Chronic wounds are associated with significant morbidity and mortality, which demand long-term effective treatment and represent a tremendous financial strain on the global healthcare systems. Regenerative medicines using stem cells have recently become apparent as a promising approach and are an active zone of investigation. They hold the potential to differentiate into specific types of cells and thus possess self-renewable, regenerative, and immune-modulatory effects. Furthermore, with the rise of technology, various cell therapies and cell types such as Bone Marrow and Adipose-derived Mesenchymal Cell (ADMSC), Endothelial Progenitor Cells (EPCs), Embryonic Stem Cells (ESCs), Mesenchymal Stem Cell (MSCs), and Pluripotent Stem Cells (PSCs) are studied for their therapeutic impact on reparative processes and tissue regeneration. Cell therapy has proven to have substantial control over enhancing the quality and rate of skin regeneration and wound restoration. The literature review brings to light the mechanics of wound healing, abnormalities resulting in chronic wounds, and the obstacles wound care researchers face, thus exploring the multitude of opportunities for potential improvement. Also, the review is focused on providing particulars on the possible cell-derived therapeutic choices and their associated challenges in healing, in the context of clinical trials, as solutions to these challenges will provide fresh and better future opportunities for improved study design and therefore yield a substantial amount of data for the development of more specialized treatments.

Fibrosis and pneumonitis are the most important side effects of lung tissue following cancer therapy. Radiotherapy and chemotherapy by some drugs, such as bleomycin, can induce pneumonitis and fibrosis. Targeted therapy and immunotherapy also may induce pneumonitis and fibrosis to a lesser extent compared to chemotherapy and radiotherapy. Activation of lymphocytes by immunotherapy or infiltration of inflammatory cells such as macrophages, lymphocytes, neutrophils, and mast cells following chemo/radiation therapy can induce pneumonitis. Furthermore, the polarization of macrophages toward M2 cells and the release of anti-inflammatory cytokines stimulate fibrosis. Lung fibrosis and pneumonitis may also be potentiated by some other changes such as epithelial-mesenchymal transition (EMT), oxidative stress, reduction/oxidation (redox) responses, renin-angiotensin system, and the upregulation of some inflammatory mediators such as a nuclear factor of kappa B (NF-ΚB), inflammasome, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). Damages to the lung vascular system and the induction of hypoxia also can induce pulmonary injury following chemo/radiation therapy. This review explains various mechanisms of the induction of pneumonitis and lung fibrosis following cancer therapy. Furthermore, the targets and promising agents to mitigate lung fibrosis and pneumonitis will be discussed.

Ischemia-reperfusion injury is a complex hemodynamic pathology that is a leading cause of death worldwide and occurs in many body organs. Numerous studies have shown that mitochondria play an important role in the occurrence mechanism of ischemia-reperfusion injury and that mitochondrial structural abnormalities and dysfunction lead to the disruption of the homeostasis of the whole mitochondria. At this time, mitochondria are not just sub-organelles to produce ATP but also important targets for regulating ischemia-reperfusion injury; therefore, drugs targeting mitochondria can serve as a new strategy to treat ischemia-reperfusion injury. Based on this view, in this review, we discuss potential therapeutic agents for both mitochondrial structural abnormalities and mitochondrial dysfunction, highlighting the application and prospects of targeted mitochondrial drugs in the treatment of ischemia-reperfusion injury, and try to provide new ideas for the clinical treatment of the ischemia-reperfusion injury.