ArticleJournal of neurotrauma2018
Post-Injury Treatment with NIM811 Promotes Recovery of Function in Adult Female Rats after Spinal Cord Contusion: A Dose-Response Study.
Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Protein-protein interaction-mediated signaling networks in ischemic stroke: from molecular mechanisms to therapeutic strategies.Acta pharmacologica Sinica · 2026Review
- Nervous System Response to Neurotrauma: A Narrative Review of Cerebrovascular and Cellular Changes After Neurotrauma.Journal of molecular neuroscience : MN · 2024Review
- Human Mesenchymal Stem Cell Transplantation Improved Functional Outcomes Following Spinal Cord Injury Concomitantly with Neuroblast Regeneration.Advanced pharmaceutical bulletin · 2023Article
- Current and future therapeutic strategies for Alzheimer's disease: an overview of drug development bottlenecks.Frontiers in aging neuroscience · 2023Review
- [Advances of the role of mitochondrial dysfunction in the spinal cord injury and its relevant treatments].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2022Review
- Secondary Mechanisms of Neurotrauma: A Closer Look at the Evidence.Diseases (Basel, Switzerland) · 2022Review
- Mitochondrial function in spinal cord injury and regeneration.Cellular and molecular life sciences : CMLS · 2022Review
- Rescuing mitochondria in traumatic brain injury and intracerebral hemorrhages - A potential therapeutic approach.Neurochemistry international · 2021Review
- Genetic Approach to Elucidate the Role of Cyclophilin D in Traumatic Brain Injury Pathology.Cells · 2021Article
- Targeting the Mitochondrial Permeability Transition Pore to Prevent Age-Associated Cell Damage and Neurodegeneration.Oxidative medicine and cellular longevity · 2021Review
- Paths to Successful Translation of New Therapies for Severe Traumatic Brain Injury in the Golden Age of Traumatic Brain Injury Research: A Pittsburgh Vision.Journal of neurotrauma · 2020Review
- Regenerative Therapies for Spinal Cord Injury.Tissue engineering. Part B, Reviews · 2019Review
- CNB-001 reduces paraplegia in rabbits following spinal cord ischemia.Neural regeneration research · 2019Article
- Pharmacological Stimulation of Mitochondrial Biogenesis Using the Food and Drug Administration-Approved βJournal of neurotrauma · 2019Article
- Targeting the mitochondrial permeability transition pore in traumatic central nervous system injury.Neural regeneration research · 2018Review
- Polycaprolactone electrospun fiber scaffold loaded with iPSCs-NSCs and ASCs as a novel tissue engineering scaffold for the treatment of spinal cord injury.International journal of nanomedicine · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial homeostasis is essential for maintaining cellular function and survival in the central nervous system (CNS). Mitochondrial function is significantly compromised after spinal cord injury (SCI) and is associated with accumulation of high levels of calcium, increased production of free radicals, oxidative damage, and eventually mitochondrial permeability transition (mPT). The formation of the mPT pore (mPTP) and subsequent mPT state are considered to be end stage events in the decline of mitochondrial integrity, and strategies that inhibit mPT can limit mitochondrial demise. Cyclosporine A (CsA) is thought to inhibit mPT by binding to cyclophilin D and has been shown to be effective in models of CNS injury. CsA, however, also inhibits calcineurin, which is responsible for its immunosuppressive properties. In the present study, we conducted a dose-response examination of NIM811, a nonimmunosuppressive CsA analog, on recovery of function and tissue sparing in a rat model of moderate to severe SCI. The results of our experiments revealed that NIM811 (10 mg/kg) significantly improved open field locomotor performance, while the two higher doses tested (20 and 40 mg/kg) significantly improved return of reflexive bladder control and significantly decreased the rostral-caudal extent of the lesion. Taken together, these results demonstrate the ability of NIM811 to improve recovery of function in SCI and support the role of protecting mitochondrial function as a potential therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.