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Biomedicines
Special Issues
Pharmacological Targets in Inflammation: Advanced Research
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Pharmacological Targets in Inflammation: Advanced Research

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 2438

Special Issue Editors

Dr. Po-Jen Chen

E-Mail Website
Guest Editor
Department of Medical Research, E-Da Hospital, Kaohsiung 824410, Taiwan
Interests: Inflammation pharmacology; Drug discovery; Cancer biology
Special Issues, Collections and Topics in MDPI journals
Dr. Kuei-Hung Lai

E-Mail Website
Guest Editor
Graduate Institute of Pharmacognosy, College of Pharmacy, Taipei Medical University, Taipei, Taiwan
Interests: natural products chemistry; drug development; functional and healthy food development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Special Issue "Pharmacological Targets in Inflammation: Advanced Research" focuses on experimental/laboratory medicine aspects of inflammation. It aims to showcase innovative research on mechanisms, pathways, and therapeutic targets in inflammation. We invite original research articles, reviews, and perspectives on the discovery, development, and evaluation of novel pharmacological targets in preclinical models and experimental settings. This Special Issue provides a platform for researchers to share their work, foster collaboration, and contribute to advancing pharmacological targets in inflammation.

Dr. Po-Jen Chen
Dr. Kuei-Hung Lai
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • inflammation
  • molecular mechanisms
  • drug discovery
  • signaling pathways
  • therapeutic strategies
  • inflammatory and autoimmune diseases
  • drug targets

Published Papers (2 papers)

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Research

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13 pages, 2793 KiB  
Article
Metabolomic Profiling of Mice with Tacrolimus-Induced Nephrotoxicity: Carnitine Deficiency in Renal Tissue
by Sho Nishida, Tamaki Ishima, Natsuka Kimura, Daiki Iwami, Ryozo Nagai, Yasushi Imai and Kenichi Aizawa
Biomedicines 2024, 12(3), 521; https://doi.org/10.3390/biomedicines12030521 - 26 Feb 2024
Viewed by 760
Abstract
Tacrolimus (TAC)-induced chronic nephrotoxicity (TAC nephrotoxicity) has a detrimental effect on long-term kidney graft survival. However, the pathogenesis of TAC nephrotoxicity remains largely unknown. We explored it by focusing on metabolic changes in renal tissues. In this study, mice were separated into TAC [...] Read more.
Tacrolimus (TAC)-induced chronic nephrotoxicity (TAC nephrotoxicity) has a detrimental effect on long-term kidney graft survival. However, the pathogenesis of TAC nephrotoxicity remains largely unknown. We explored it by focusing on metabolic changes in renal tissues. In this study, mice were separated into TAC and control groups (n = 5/group). TAC was administered to the TAC group (1 mg/kg/d for 28 days) subcutaneously. The control group was similarly treated with normal saline. Renal tissue metabolomes were evaluated. Renal fibrosis was observed only in the TAC group. Metabolomic analysis showed that carnitine and related metabolites were substantially lower in the TAC group than in the control group, presumably due to impaired biosynthesis and reabsorption. Low carnitine levels impair antioxidation in renal tissues and β-oxidation in mitochondria, which may lead to renal tissue damage. This metabolomic analysis revealed that carnitine deficiency in renal tissue appears to explain TAC nephrotoxicity. Full article
(This article belongs to the Special Issue Pharmacological Targets in Inflammation: Advanced Research)
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14 pages, 1286 KiB  
Opinion
Targeting TLR Signaling Cascades in Systemic Lupus Erythematosus and Rheumatoid Arthritis: An Update
by George D. Kalliolias, Efthimia K. Basdra and Athanasios G. Papavassiliou
Biomedicines 2024, 12(1), 138; https://doi.org/10.3390/biomedicines12010138 - 09 Jan 2024
Viewed by 1374
Abstract
Evidence from animal models and human genetics implicates Toll-like Receptors (TLRs) in the pathogenesis of Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Endosomal TLRs sensing nucleic acids were proposed to induce lupus-promoting signaling in dendritic cells, B cells, monocytes, and macrophages. Ligation [...] Read more.
Evidence from animal models and human genetics implicates Toll-like Receptors (TLRs) in the pathogenesis of Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). Endosomal TLRs sensing nucleic acids were proposed to induce lupus-promoting signaling in dendritic cells, B cells, monocytes, and macrophages. Ligation of TLR4 in synovial macrophages and fibroblast-like synoviocytes (FLSs) by endogenous ligands was suggested to induce local production of mediators that amplify RA synovitis. Inhibition of TLRs using antagonists or monoclonal antibodies (mAbs) that selectively prevent extracellular or endosomal TLR ligation has emerged as an attractive treatment strategy for SLE and RA. Despite the consistent success of selective inhibition of TLR ligation in animal models, DV-1179 (dual TLR7/9 antagonist) failed to achieve pharmacodynamic effectiveness in SLE, and NI-0101 (mAb against TLR4) failed to improve arthritis in RA. Synergistic cooperation between TLRs and functional redundancy in human diseases may require pharmacologic targeting of intracellular molecules that integrate signaling downstream of multiple TLRs. Small molecules inhibiting shared kinases involved in TLR signaling and peptidomimetics disrupting the assembly of common signalosomes (“Myddosome”) are under development. Targeted degraders (proteolysis-targeting chimeras (PROTACs)) of intracellular molecules involved in TLR signaling are a new class of TLR inhibitors with promising preliminary data awaiting further clinical validation. Full article
(This article belongs to the Special Issue Pharmacological Targets in Inflammation: Advanced Research)
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