Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
6.8
3.9
Journals
Biomedicines
Special Issues
Traumatic CNS Injury: From Bench to Bedside (2nd Edition)
share announcement

Traumatic CNS Injury: From Bench to Bedside (2nd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 6498

Special Issue Editor

Prof. Dr. Andres M. Rubiano

E-Mail Website
Guest Editor
Neurosciences Institute, INUB-MEDITECH Research Group, El Bosque University, 113033 Bogotá, Colombia
Interests: trauma; neurotrauma; prehospital care; emergency care; critical care; trauma surgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the field of CNS traumatic injury, taking results from the laboratory into the clinic that can directly benefit patients is often a very lengthy and complex process.

In recent decades, several areas linked to the care of these patients have evolved from the diagnosis point to medical and surgical care. The introduction of biomarkers and new technological devices for the better selection of the most critical patients has shown a trend towards more precise treatment pathways.

Additionally, recent clinical studies, involving medical and surgical therapies, have also shown which interventions definitively work or not and how they can be managed in different contexts.

This linear process seems straightforward, but we all know how many barriers can be met in the scientific process. Issues related to methodological designs and selection bias and difficulties with preclinical models can be associated with different impacts over the results.

The aim of this Special Issue is to provide an opportunity to share different kinds of primary and secondary studies where all aspects of the translation of science can be highlighted, focusing on detailed information for scientists dedicated to the care of these patients worldwide, in different settings, and with different levels of resource availability.

Prof. Dr. Andres M. Rubiano
Guest Editor

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

  • neurotrauma
  • traumatic brain injury
  • translational science
  • bench to bedside
  • neuroprotection

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Related Special Issue

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 744 KB  
Article
Early Thrombocytopenia at Hospital Admission Predicts Mortality in Patients with Non-Isolated Severe Traumatic Brain Injury
by Patricia Piñeiro, Alberto Calvo, María Dolores Pérez-Díaz, Silvia Ramos, Sergio García-Ramos, Mercedes Power, Isabel Solchaga, Cristina Rey, Javier Hortal, Fernando Turégano and Ignacio Garutti
Biomedicines 2024, 12(12), 2702; https://doi.org/10.3390/biomedicines12122702 - 26 Nov 2024
Viewed by 1378
Abstract
Patients with severe traumatic brain injury (STBI) often experience an abnormal hemostasis that contributes to mortality and unfavorable neurological outcomes. Objectives: We aimed to analyze epidemiologic, clinical, and laboratory factors associated with mortality in patients with STBI during the first 48 h after [...] Read more.
Patients with severe traumatic brain injury (STBI) often experience an abnormal hemostasis that contributes to mortality and unfavorable neurological outcomes. Objectives: We aimed to analyze epidemiologic, clinical, and laboratory factors associated with mortality in patients with STBI during the first 48 h after in-hospital admission. Methods: We performed an observational retrospective study of STBI patients with associated extracranial trauma [defined as Injury Severity Score (ISS) ≥ 16 with an Abbreviated Injury Scale (AIS) head and neck ≥ 3 and Glasgow Coma Scale (GCS) ≤ 8] admitted to a Level II trauma center over seven years (2015–2021). Patients were divided into two groups: survivors and dead. We assessed differences regarding demographics, trauma severity, hemodynamics, disability, need for surgery, length of stay, transfusions, need for massive transfusion protocol, and hemostatic laboratory parameters at different time points. Results: A total of 134 STBI patients were included. Patients who died were older, mostly men, and showed higher trauma severity and disability. Hemoglobin, platelets, and clotting parameters deteriorated after admission to the emergency department (ED) with significant differences between groups within the first 24 h after admission. Platelet count < 150 × 103/μL at ED arrival, GCS, and age were independent risk factors for mortality. Conclusions: Older age, GCS, and platelet count at ED arrival were independent risk factors for mortality in STBI patients with associated extracranial trauma. Early thrombocytopenia < 150 × 103/μL at ED arrival may be used as a simple prognostic tool to early predict mortality between non-isolated STBI. Full article
(This article belongs to the Special Issue Traumatic CNS Injury: From Bench to Bedside (2nd Edition))
►▼ Show Figures

Graphical abstract

Review

Jump to: Research

17 pages, 723 KB  
Review
Rebuilding Mitochondrial Homeostasis and Inhibiting Ferroptosis: Therapeutic Mechanisms and Prospects for Spinal Cord Injury
by Qin Wang, Qingqing Qin, Wenqiang Liang, Haoran Guo, Yang Diao, Shengsheng Tian and Xin Wang
Biomedicines 2025, 13(9), 2290; https://doi.org/10.3390/biomedicines13092290 - 18 Sep 2025
Viewed by 463
Abstract
During the pathological process of spinal cord injury (SCI), ferroptosis is closely related to mitochondrial homeostasis. Following the occurrence of SCI, the interruption of local blood supply leads to mitochondrial damage within cells and a reduction in Adenosine triphosphate (ATP) production. This results [...] Read more.
During the pathological process of spinal cord injury (SCI), ferroptosis is closely related to mitochondrial homeostasis. Following the occurrence of SCI, the interruption of local blood supply leads to mitochondrial damage within cells and a reduction in Adenosine triphosphate (ATP) production. This results in the loss of transmembrane ion gradients, causing an influx of Ca2+ into the cells, which in turn generates a significant amount of Reactive oxygen species (ROS) and reactive nitrogen species. This leads to severe mitochondrial dysfunction and an imbalance in mitochondrial homeostasis. Ferroptosis is a form of programmed cell death that differs from other types of apoptosis, as it is dependent on the accumulation of iron and lipid peroxides, along with their byproducts. The double bond structures in intracellular polyunsaturated fatty acids (PUFA) are particularly susceptible to attack by ROS, leading to the formation of lipid alkyl free radicals. This accumulation of lipid peroxides within the cells triggers ferroptosis. After SCI, the triggering of ferroptosis is closely associated with the “death triangle”—a core network that catalyzes cell death through the interaction of three factors: local iron overload, collapse of antioxidant defenses, and dysregulation of PUFA metabolism (where PUFA are susceptible to attack by reactive ROS leading to lipid peroxidation). These three elements interact to form a central network driving cell death. In the pathological cascade of SCI, mitochondria serve as both a major source of ROS and a primary target of their attack, playing a crucial role in the initiation and execution of cellular ferroptosis. Mitochondrial homeostasis imbalance is not only a key inducer of the “death triangle” (such as the intensification of lipid peroxidation by mitochondrial ROS), but is also reverse-regulated by the “death triangle” (such as the destruction of mitochondrial structure by lipid peroxidation products). Through the cascade reaction of this triangular network, mitochondrial homeostasis imbalance and the “death triangle” jointly drive the progression of secondary damage. This study aims to synthesize the mechanisms by which various therapeutic approaches mitigate SCI through targeted regulation of mitochondrial homeostasis and inhibition of ferroptosis. Unlike previous research, we integrate the bidirectional regulatory relationship between “mitochondrial homeostasis disruption” and “ferroptosis” in SCI, and emphasize their importance as a synergistic therapeutic target. We not only elaborate in detail how mitochondrial homeostasis—including biogenesis, dynamics, and mitophagy—modulates the initiation and execution of ferroptosis, but also summarize recent strategies that simultaneously target both processes to achieve neuroprotection and functional recovery. Furthermore, this review highlights the translational potential of various treatments in blocking the pathological cascade driven by oxidative stress and lipid peroxidation. These insights provide a novel theoretical framework and propose combinatory therapeutic approaches, thereby laying the groundwork for designing precise and effective comprehensive treatment strategies for SCI in clinical settings. Full article
(This article belongs to the Special Issue Traumatic CNS Injury: From Bench to Bedside (2nd Edition))
►▼ Show Figures

Graphical abstract

18 pages, 2633 KB  
Review
Cerebral Edema in Traumatic Brain Injury
by Santiago Cardona-Collazos, Wendy D. Gonzalez, Pamela Pabon-Tsukamoto, Guo-Yi Gao, Alexander Younsi, Wellingson S. Paiva and Andres M. Rubiano
Biomedicines 2025, 13(7), 1728; https://doi.org/10.3390/biomedicines13071728 - 15 Jul 2025
Cited by 2 | Viewed by 4186
Abstract
Cerebral edema is the abnormal accumulation of fluid in any of the tissue compartments of the cerebral parenchyma. It remains a significant challenge in neurotrauma care because it contributes to secondary brain injury, affecting prognosis. This review analyzes the recent literature, including foundational [...] Read more.
Cerebral edema is the abnormal accumulation of fluid in any of the tissue compartments of the cerebral parenchyma. It remains a significant challenge in neurotrauma care because it contributes to secondary brain injury, affecting prognosis. This review analyzes the recent literature, including foundational studies, to describe the mechanisms of distinct types of cerebral edema following traumatic brain injury (TBI). Emerging concepts, such as the role of the glymphatic system and heme-derived inflammasomes, offer new insights into new types of edemas, differentiated by pathogenesis and potential treatments. Recent advancements in understanding these molecular mechanisms can improve therapeutic strategies, facilitating a better approach in the era of precision and personalized medicine. Although there has been notable progress, a proposal to customize treatments for diverse types of edemas is necessary to improve outcomes following traumatic brain injury. In this review, we describe the current subtypes of post-traumatic brain edemas and link them to a specific management approach. Full article
(This article belongs to the Special Issue Traumatic CNS Injury: From Bench to Bedside (2nd Edition))
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop