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Targeting Metabolism, Inflammation, and Oxidative Stress: Novel Therapeutic Approaches in Human Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 334

Editor


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Guest Editor
Department of Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT 84606, USA
Interests: oxidative stress-induced signal transduction mechanisms; pathophysiology of secondary diabetic complications; carcinogenesis; inflammatory complications; therapeutic development of small molecular inhibitors and antioxidants

Special Issue Information

Dear Colleagues,

Modulating metabolism, inflammation, and oxidative stress is essential for managing various human diseases. Numerous recent studies have demonstrated strong links between cellular metabolism, inflammation, and oxidative stress, which contribute to the pathophysiology of conditions such as diabetes, aging, cardiovascular diseases, neurological disorders, and cancer. Strategies targeting these processes could offer therapeutic benefits. Specifically, dietary interventions, pharmacological agents, anti-inflammatory drugs, and lifestyle modifications like regular exercise and stress reduction can help control disease development and progression. Additionally, nutritional supplements, natural antioxidants, and phytochemicals that regulate various molecular signaling pathways may play crucial preventive roles in disease control. Emerging therapies, including gene editing, stem cell therapy, next-generation sequencing, regenerative medicine, and microbiome manipulation, show promise in modulating cellular metabolism, inflammatory responses, and oxidative stress for future treatments.

This Special Issue aims to provide an updated overview of the complex interplay between metabolic imbalance, chronic inflammation, and oxidative stress in the pathophysiology of human diseases. It invites contributions in the form of structural and computational studies, functional analyses, preclinical and clinical research, and comprehensive reviews, focusing on novel strategies targeting metabolism, inflammation, and oxidative stress to control various human pathologies.

Dr. Kota V. Ramana
Guest Editor

Manuscript Submission Information

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Keywords

  • metabolism 
  • inflammation 
  • oxidative stress 
  • diabetes 
  • aging 
  • cardiovascular diseases 
  • gene editing 
  • stem cell therapy 
  • next-generation sequencing 
  • regenerative medicine

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Published Papers (1 paper)

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Research

21 pages, 2594 KB  
Article
In Vivo Efficacy of an Inhibitor of Complement and FcRn in Models of Glomerulonephritis and Collagen-Induced Arthritis Using Human C2 Knock-In Mice
by Helen Cao, Amelia Nash, Yun Dai, Arthur Hsu, Amanda L. Turner, Kaushala Jayawardana, Sharon Vyas, Adele Barr, Sandra Wymann and Matthew P. Hardy
Int. J. Mol. Sci. 2026, 27(12), 5525; https://doi.org/10.3390/ijms27125525 (registering DOI) - 18 Jun 2026
Viewed by 144
Abstract
A therapeutic antibody, CSL305, has been developed, which combines inhibition of the complement classical and lectin pathways via complement C2 binding with an ability to act as an antagonist of the neonatal Fc receptor (FcRn). CSL305 binds to human C2 (huC2) but shows [...] Read more.
A therapeutic antibody, CSL305, has been developed, which combines inhibition of the complement classical and lectin pathways via complement C2 binding with an ability to act as an antagonist of the neonatal Fc receptor (FcRn). CSL305 binds to human C2 (huC2) but shows no binding or activity against mouse C2 precluding its use in mouse models of disease to fully assess in vivo efficacy. To circumvent this, a mouse strain was developed that replaced the expression of mouse C2 with huC2 by homologous recombination. These mice (huC2 “knock-in”; KI) were shown to express huC2 protein and to have complement activity. Interestingly, male huC2-KI mice showed much stronger complement activity compared to female mice and were also sensitive to inhibition by CSL305. Two models of disease using male huC2-KI mice were then used to assess the in vivo efficacy of CSL305. The first was an attenuated passive anti-glomerular basement membrane (GBM) glomerulonephritis model involving complement activation as its primary mechanism of action. CSL305 showed dose-dependent inhibition of disease as measured by urine albumin, with reductions in kidney cellular infiltration and plasma C3 cleaved fragments C3b/C3c/iC3b also observed. The second model was a collagen autoantibody-induced arthritis (CAIA) mouse model. Here, CSL305 showed a significant and dose-dependent inhibition of clinical score in both prophylactic and therapeutic settings, mediated exclusively via its FcRn mechanism of action. Although the animal models used in this study were found to preclude the demonstration of a synergistic effect on both mechanisms, CSL305 does act in vivo as both a complement inhibitor and as a FcRn antagonist to ameliorate disease. Full article
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