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Biomolecules
Special Issues
Advancing Innovations in Biomedical Research for Translational Applications
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Advancing Innovations in Biomedical Research for Translational Applications

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 3054

Special Issue Editors

Prof. Dr. Jianjie Ma

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Guest Editor
School of Medicine, University of Virginia, Charlottesville, VA 22903, USA
Interests: muscle physiology and cardiovascular diseases; regenerative medicine; immune regulation; therapeutic development
Special Issues, Collections and Topics in MDPI journals
Dr. Ki Ho Park

E-Mail Website
Guest Editor
Division of Surgical Sciences, Department of Surgery, University of Virginia, Charlottesville, VA 22903, USA
Interests: vascular biology; vascular remodeling; muscle physiology; ion channels; protein therapeutics; regenerative medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Zui Pan

E-Mail Website
Guest Editor
Department of Graduate Nursing, Bone-Muscle Research Center, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX, USA
Interests: calcium signaling and its pathophysiological implications in human diseases; live cell imaging; molecular gene modulation; transgenic animal models

Special Issue Information

Dear Colleagues,

Innovations in biomedical research continue to drive translational breakthroughs across a wide spectrum of human diseases. Over the past decades, remarkable progress has been made in areas such as nanoparticle-mediated delivery systems that enable precision medicine, advanced proteomic and lipidomic profiling techniques that uncover the molecular basis of diseases, and cutting-edge tools designed to enhance stem cell function in aging and degenerative conditions. In parallel with these advancements, the development of novel therapeutic strategies, including targeted delivery of recombinant proteins, monoclonal antibodies, natural products, and engineered stem cells, has opened new frontiers for combating human diseases.

In this Special Issue, “Advancing Innovations in Biomedical Research for Translational Applications”, we aim to highlight multidisciplinary approaches at the forefront of biomedical innovation that are paving the way toward impactful therapeutic applications. We invite original research articles and comprehensive reviews that align with the following key themes:

  • Nanoparticle-based drug delivery for precision medicine;
  • Integrative bioengineering approaches to rejuvenate stem cell function;
  • Proteomic and lipidomic profiling for disease mechanism discovery;
  • Novel therapeutic strategies in regenerative medicine;
  • Biologic drug development from discovery to IND submission.

We particularly encourage contributions from early-career investigators and emerging leaders in translational biomedical research. Your participation will help to shape this exciting Special Issue and inspire future directions in the field.

Prof. Dr. Jianjie Ma
Dr. Ki Ho Park
Dr. Zui Pan
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. Biomolecules 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 2700 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

  • nanoparticle drug delivery
  • precision medicine
  • stem cell
  • proteomic and lipidomic profiling
  • novel therapeutic strategies
  • regenerative medicine
  • biologic drug development
  • IND submission

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

12 pages, 1439 KB  
Article
Humanized Monoclonal Antibody Against Citrullinated Histone H3 Attenuates Myocardial Injury and Prevents Heart Failure in Rodent Models
by Matthew Weber, Yuchen Chen, Xinyu Zhou, Heejae Chun, Di Wu, Ki Ho Park, Chuanxi Cai, Yongqing Li, Jianjie Ma and Zequan Yang
Biomolecules 2025, 15(8), 1196; https://doi.org/10.3390/biom15081196 - 20 Aug 2025
Viewed by 871
Abstract
Background: Excessive formation of neutrophil extracellular traps (NETs) leads to NETosis, accompanied by the release of citrullinated histone H3 (CitH3), a key mediator of septic inflammation. However, the role of CitH3 in sterile inflammation, such as acute myocardial infarction (MI) and post-MI heart [...] Read more.
Background: Excessive formation of neutrophil extracellular traps (NETs) leads to NETosis, accompanied by the release of citrullinated histone H3 (CitH3), a key mediator of septic inflammation. However, the role of CitH3 in sterile inflammation, such as acute myocardial infarction (MI) and post-MI heart failure, remains incompletely understood. Methods and Results: We investigated the role of CitH3, a byproduct of NETosis, in myocardial ischemia/reperfusion (I/R) injury using a murine MI model. C57BL/6J mice were subjected to left coronary artery (LCA) occlusion followed by reperfusion and treated with either a humanized anti-CitH3 monoclonal antibody (hCitH3-mAb) or control human IgG. In mice undergoing 40 min of LCA occlusion and 24 h of reperfusion, hCitH3-mAb administered 10 min before reperfusion significantly reduced infarct size by 36% compared to control (p < 0.05). Plasma levels of CitH3, IL-1β, and interferon-β were significantly elevated following MI but were attenuated by hCitH3-mAb. In addition, plasma and cardiac tissue from treated mice showed significantly lower levels of citrate synthase, a marker of mitochondrial injury, suggesting that hCitH3-mAb preserved mitochondrial integrity after MI. In mice undergoing 50 min of LCA occlusion and 21 days of reperfusion, longitudinal echocardiography revealed preservation of left ventricular ejection fraction (LVEF) in hCitH3-mAb-treated mice, with significant improvement observed on days 7, 14, and 21 post-MI (p < 0.05 vs. control). hCitH3-mAb also mitigated myocardial fibrosis and preserved tissue architecture. Conclusions: These findings demonstrated CitH3 as a critical mediator of myocardial injury and adverse remodeling following acute MI. Neutralization of CitH3 via hCitH3-mAb attenuates I/R injury and preserves cardiac function by mitigating inflammation and protecting mitochondrial integrity. Targeting CitH3 represents a promising therapeutic strategy to prevent heart failure following MI. Full article
(This article belongs to the Special Issue Advancing Innovations in Biomedical Research for Translational Applications)
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24 pages, 2944 KB  
Article
Oral Pharmacokinetic Evaluation of a Microemulsion-Based Delivery System for Novel A190 Prodrugs
by Sagun Poudel, Chaolong Qin, Rudra Pangeni, Ziwei Hu, Grant Berkbigler, Madeline Gunawardena, Adam S. Duerfeldt and Qingguo Xu
Biomolecules 2025, 15(8), 1101; https://doi.org/10.3390/biom15081101 - 30 Jul 2025
Viewed by 1024
Abstract
Peroxisome proliferator-activated receptor alpha (PPARα) is a key regulator of lipid metabolism, making its agonists valuable therapeutic targets for various diseases, including chronic peripheral neuropathy. Existing PPARα agonists face limitations such as poor selectivity, sub-optimal bioavailability, and safety concerns. We previously demonstrated that [...] Read more.
Peroxisome proliferator-activated receptor alpha (PPARα) is a key regulator of lipid metabolism, making its agonists valuable therapeutic targets for various diseases, including chronic peripheral neuropathy. Existing PPARα agonists face limitations such as poor selectivity, sub-optimal bioavailability, and safety concerns. We previously demonstrated that A190, a novel, potent, and selective PPARα agonist, effectively alleviates chemotherapy-induced peripheral neuropathy and CFA-induced inflammatory pain as a non-opioid therapeutic agent. However, A190 alone has solubility and permeability issues that limits its oral delivery. To overcome this challenge, in this study, four new-generation ester prodrugs of A190; A190-PD-9 (methyl ester), A190-PD-14 (ethyl ester), A190-PD-154 (isopropyl ester), and A190-PD-60 (cyclic carbonate) were synthesized and evaluated for their enzymatic bioconversion and chemical stability. The lead candidate, A190-PD-60, was further formulated as a microemulsion (A190-PD-60-ME) and optimized via Box–Behnken design. A190-PD-60-ME featured nano-sized droplets (~120 nm), low polydispersity (PDI < 0.3), and high drug loading (>90%) with significant improvement in artificial membrane permeability. Crucially, pharmacokinetic evaluation in rats demonstrated that A190-PD-60-ME reached a 16.6-fold higher Cmax (439 ng/mL) and a 5.9-fold increase in relative oral bioavailability compared with an A190-PD-60 dispersion. These findings support the combined prodrug-microemulsion approach as a promising strategy to overcome oral bioavailability challenges and advance PPARα-targeted therapies. Full article
(This article belongs to the Special Issue Advancing Innovations in Biomedical Research for Translational Applications)
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15 pages, 4150 KB  
Article
PRMT5 Identified as a Viable Target for Combination Therapy in Preclinical Models of Pancreatic Cancer
by Xiaolong Wei, William J. Kane, Sara J. Adair, Sarbajeet Nagdas, Denis Liu and Todd W. Bauer
Biomolecules 2025, 15(7), 948; https://doi.org/10.3390/biom15070948 - 30 Jun 2025
Viewed by 801
Abstract
Pancreatic cancer is the third leading cause of cancer-related death in the US. First-line chemotherapy regimens for pancreatic ductal adenocarcinoma (PDAC) include FOLFIRINOX or gemcitabine (Gem) with or without paclitaxel (Ptx); however, 5-year survival with these regimens remains poor. Previous work has demonstrated [...] Read more.
Pancreatic cancer is the third leading cause of cancer-related death in the US. First-line chemotherapy regimens for pancreatic ductal adenocarcinoma (PDAC) include FOLFIRINOX or gemcitabine (Gem) with or without paclitaxel (Ptx); however, 5-year survival with these regimens remains poor. Previous work has demonstrated protein arginine methyltransferase 5 (PRMT5) to be a promising therapeutic target in combination with Gem for the treatment of PDAC; however, these findings have yet to be confirmed in relevant preclinical models of PDAC. To test the possibility of PRMT5 as a viable therapeutic target, clinically relevant orthotopic and metastatic patient-derived xenograft (PDX) mouse models of PDAC growth were utilized to evaluate the effect of PRMT5 knockout (KO) or pharmacologic inhibition on treatment with Gem alone or Gem with Ptx. Primary endpoints included tumor volume, tumor weight, or metastatic tumor burden as appropriate. The results showed that Gem-treated PRMT5 KO tumors exhibited decreased growth and were smaller in size compared to Gem-treated wild-type (WT) tumors. Similarly, the Gem-treated PRMT5 KO metastatic burden was lower than the Gem-treated WT metastatic burden. The addition of a PRMT5 pharmacologic inhibitor to Gem and Ptx therapy resulted in a lower final tumor weight and fewer metastatic tumors. The depletion of PRMT5 results in increased DNA damage in response to Gem and Ptx treatment. Thus, PRMT5 genetic depletion or inhibition in combination with Gem-based therapy improved the response in primary and metastatic PDAC in clinically relevant mouse models, suggesting that PRMT5 is a viable therapeutic target for combination therapy in PDAC. Full article
(This article belongs to the Special Issue Advancing Innovations in Biomedical Research for Translational Applications)
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