Current drug targets最新文献

Background: Cancer involves uncontrolled cell growth due to genetic mutations. Tumors can form when CDK6, a gene essential for controlling cell growth, isn't working correctly. Researchers are investigating drugs that inhibit CDK6; some of them appear promising. Nevertheless, CDK6 is advantageous and harmful to cancer because it controls other cellular processes. By inhibiting CDK6 and CDK4, CDK4/6 inhibitors offer a novel therapeutic strategy that stops cell proliferation. The study investigates the function of CDK6 in cancer, the difficulties in targeting CDK6, and possible remedies.

Objective: Scientists have developed drugs designed to block CDK6 and prevent it from altering other proteins. These drugs, also known as CDK6 inhibitors, help treat cancer. Finding the best drugs for CDK6 is still tricky, though. The drugs' selectivity, potency, and cost are some difficulties. These factors depend on CDK6's structure and interactions with other proteins. The structure of CDK6 and how it influences its function and regulation are explained in this review. It also describes CDK6's function in cancer and its interaction with other molecules and proteins, which is crucial for cell division. This review also discusses the present and upcoming therapies that target CDK6, as well as how CDK6 interacts with drugs that block it.

Conclusion: This review presents the structure, current research, and overview of CDK6. It also reviews the role of CDK6 in cancer, function, and regulation. Additionally, it explores its role in cancer signaling networks and its interaction with CDK6 inhibitors. Lastly, it discusses the current status and prospects of therapies targeting CDK6.

The main epidemiological and clinical data on colorectal cancer, as well as the features of molecular pathology, are discussed in the literature review. Efforts are being putto identify promising targets, particularly small non-coding nucleotide sequences, which can lead to new treatments for this disease. The discovery of significant mutations that contribute to the development of colorectal tumors is a major step in the advancement of molecular oncology, as these mutations give rise to heterogeneous tumors that differ in their origin. These mutations play a significant role in the progression of the disease and are now being targeted for treatment. The prognosis for a disease is influenced by the patient's sensitivity to antitumor therapy. However, new approaches to finding effective targets for antitumor treatments face new fundamental challenges due to clinical issues. These issues include the epigenetic regulation of markers of oncogenesis, which allows for the development of new therapeutic strategies. RNA interference, in particular, has been linked to non-copying RNA sequences such as microRNAs. These microRNAs are associated with certain processes that can influence all aspects of oncogenesis. The diversity of microRNAs allows for a differentiated approach when treating tumors in various locations.

Diabetes Mellitus (DM) is referred to as hyperglycemia in either fasting or postprandial phases. Oxidative stress, which is defined by an excessive amount of reactive oxygen species (ROS) production, increased exposure to external stress, and an excessive amount of the cellular defense system against them, results in cellular damage. Increased DNA damage is one of the main causes of genomic instability, and genetic changes are an underlying factor in the emergence of cancer. Through covalent connections with DNA and proteins, quercetin has been demonstrated to offer protection against the creation of oxidative DNA damage. It has been found that quercetin shields DNA from possible oxidative stress-related harm by reducing the production of ROS. Therefore, Quercetin helps to lessen DNA damage and improve the ability of DNA repair mechanisms. This review mainly focuses on the role of quercetin in repairing DNA damage and compensating for drug resistance in diabetic patients. Data on the target topic was obtained from major scientific databases, including SpringerLink, Web of Science, Google Scholar, Medline Plus, PubMed, Science Direct, and Elsevier. In preclinical studies, quercetin guards against DNA deterioration by regulating the degree of lipid peroxidation and enhancing the antioxidant defense system. By reactivating antioxidant enzymes, decreasing ROS levels, and decreasing the levels of 8-hydroxydeoxyguanosine, Quercetin protects DNA from oxidative damage. In clinical studies, it was found that quercetin supplementation was related to increased antioxidant capacity and decreased risk of type 2 diabetes mellitus in the experimental group as compared to the placebo group. It is concluded that quercetin has a significant role in DNA repair in order to overcome drug resistance in diabetes.

Quercetin is a natural flavonoid with various pharmacological actions such as anti-inflammatory, antioxidant, antimicrobial, anticancer, antiviral, antidiabetic, cardioprotective, neuroprotective, and antiviral activities. Looking at these enormous potentials, researchers have explored how they can be used to manage numerous cancers. It's been studied for cancer management due to its anti-angiogenesis, anti-metastatic, and antiproliferative mechanisms. Despite having these proven pharmacological activities, the clinical use of quercetin is limited due to its first-- pass metabolism, poor solubility, and bioavailability. To address these shortcomings, researchers have fabricated various nanocarriers-based formulations to fight cancer. The present review overshadows the pharmacological potential, mechanisms, and application of nanoformulations against different cancers. Teaser: Explore the potential of Quercetin, a natural flavonoid with diverse pharmacological activities, and its nanoformulations in managing various cancers.

Background and aim: Diabetes mellitus is a chronic, multi-factorial metabolic disorder and also an important public health issue that requires multi-dimensional therapeutic strategies for effective control. Unani herbs have long been used to effectively mitigate diabetes through various mechanisms. In recent years, it has been speculated that the alteration of gut microbiome ecology is potentially one of the important mechanisms through which the Unani drugs exert hypoglycemic action. This review aims at the trans-disciplinary interpretation of the holistic concepts of the Unani system of medicine and the molecular insights of contemporary medicine for novel strategies for diabetes management.

Methodology: We searched scientific databases such as PubMed, Google Scholar, and Science-Direct, etc. Unani classical texts (Urdu, Arabic, and Persian), and medical books, for diabetic control with Unani medicine through the gut microbiome.

Results: Unani medicine defines, diabetes as a urinary system disorder disrupting the transformational faculty (Quwwat Mughayyira) in the gastrointestinal tract. The Unani system and contemporary biomedicine use different epistemology and ontology for describing diabetes through gutderived factors in whole-body glucose homeostasis. Unani Pharmaceutics have reported in clinical and preclinical (in vitro/ in vivo) trials in improving diabetes by altering gut microbiota composition, microvascular dysfunction, and inflammation. However, the preventive plan is the preservance of six essential factors (Asbāb Sitta Ḍarūriyya) as a lifestyle plan.

Conclusion: This is the first study on the integrative strategy about the hypoglycemic effects of Unani herbs that could serve as a prerogative novel approach for cost-effective, holistic, rationalistic, and multi-targeted diabetes management.

Parkinson's disease (PD) is a progressive neurodegenerative disorder that impacts a significant portion of the population. Despite extensive research, an effective cure for PD remains elusive, and conventional pharmacological treatments often face limitations in efficacy and management of symptoms. There has been a lot of discussion about using nanotechnology to increase the bioavailability of small- molecule drugs to target cells in recent years. It is possible that PD treatment might become far more effective and have fewer side effects if medication delivery mechanisms were to be improved. Potential alternatives to pharmacological therapy for molecular imaging and treatment of PD may lie in abnormal proteins such as parkin, α-synuclein, leucine-rich repeat serine and threonine protein kinase 2. Published research has demonstrated encouraging outcomes when nanomedicine-based approaches are used to address the challenges of PD therapy. So, to address the present difficulties of antiparkinsonian treatment, this review outlines the key issues and limitations of antiparkinsonian medications, new therapeutic strategies, and the breadth of delivery based on nanomedicine. This review covers a wide range of subjects, including drug distribution in the brain, the efficacy of drug-loaded nano-carriers in crossing the blood-brain barrier, and their release profiles. In PD, the nano-carriers are also used. Novel techniques of pharmaceutical delivery are currently made possible by vesicular carriers, which eliminate the requirement to cross the blood-brain barrier (BBB).

Gallbladder cancer (GBC) is an uncommon condition in which malignant (cancer) cells are detected in gallbladder tissue. Cancer is often triggered when normal cells turn malignant and begin to spread. Cancer can also be caused by genetic anomalies that result in uncontrolled cell proliferation and tumor development. MicroRNAs (also known as miRNAs or miRs) are a group of small, endogenous, non-coding RNAs of 19-23 nucleotides in length, which play a key role in post-transcriptional gene regulation. These miRNAs serve as negative gene regulators by supervising target genes and regulating biological processes, including cell proliferation, migration, invasion, and apoptosis. Cancer development and progression relate to aberrant miRNA expression. This review demonstrated the implication of various genetic factors and microRNAs in developing and regulating GBC. This suggests the potential of genes and RNAs as the diagnostic, prognostic, and therapeutic targets in gallbladder cancer.