Scholarlink

<p>The brain is uniquely vulnerable to mitochondrial dysfunction, a primary hallmark of neurodegenerative diseases. While mitochondria are universally recognized as cellular powerhouses, their organ-specific functional architectures remain poorly defined. In this study, we present a high-resolution transcriptomic analysis compared across cerebellar tissue (used as the neural reference) and peripheral tissues (heart, kidney, and ovary) to map the coordination of transport, signaling, and detoxification. Using ovarian tissue as a stable physiological baseline, our findings demonstrate that neural mitochondria are fundamentally architected for metabolic surveillance and repair rather than sheer bioenergetic throughput. To safely meet the extreme metabolic demands of synaptic transmission, the brain exhibits reduced transcriptional emphasis on bulk bioenergetic exchange pathways relative to signaling and repair modules in favor of three highly specialized functional pillars: tightly regulated transport (e.g., <i>SFXN4</i>, <i>SLC25A14</i>, and <i>SLC25A22</i>,<i> SLC25A25</i>), highly responsive metabolic signaling (anchored by <i>EFHD1</i> and retrograde communication), and targeted detoxification and protein repair (e.g., <i>MSRA</i> and <i>MSRB2</i>). Furthermore, phylogenetic conservation analysis comparing the bovine lineage to the human transcriptomic reference data across 90&#xa0;million years of mammalian evolution confirms that these neural-specific adaptations exhibit highly conserved expression hierarchies. This evolutionary rigidity proves that this specific neurochemical architecture is a deeply conserved, essential requirement for protecting the central nervous system. Consequently, defining this baseline establishes a critical molecular framework for identifying precise therapeutic targets to combat oxidative stress, excitotoxicity, and age-related neurodegeneration.</p> Graphical Abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The Unique Mitochondrial Architecture of the Buffalo Brain: A Comparative Transcriptomic Analysis of Transport, Signaling, and Detoxification

  • 期刊论文

  • 发表日期：

    2026年7月17日

查看全文
  • E. M. Sadeesh,
  • Madhuri S. Lahamge,
  • A. N. Ampadi,
  • Roshan Mohiddin

摘要

The brain is uniquely vulnerable to mitochondrial dysfunction, a primary hallmark of neurodegenerative diseases. While mitochondria are universally recognized as cellular powerhouses, their organ-specific functional architectures remain poorly defined. In this study, we present a high-resolution transcriptomic analysis compared across cerebellar tissue (used as the neural reference) and peripheral tissues (heart, kidney, and ovary) to map the coordination of transport, signaling, and detoxification. Using ovarian tissue as a stable physiological baseline, our findings demonstrate that neural mitochondria are fundamentally architected for metabolic surveillance and repair rather than sheer bioenergetic throughput. To safely meet the extreme metabolic demands of synaptic transmission, the brain exhibits reduced transcriptional emphasis on bulk bioenergetic exchange pathways relative to signaling and repair modules in favor of three highly specialized functional pillars: tightly regulated transport (e.g., SFXN4, SLC25A14, and SLC25A22, SLC25A25), highly responsive metabolic signaling (anchored by EFHD1 and retrograde communication), and targeted detoxification and protein repair (e.g., MSRA and MSRB2). Furthermore, phylogenetic conservation analysis comparing the bovine lineage to the human transcriptomic reference data across 90 million years of mammalian evolution confirms that these neural-specific adaptations exhibit highly conserved expression hierarchies. This evolutionary rigidity proves that this specific neurochemical architecture is a deeply conserved, essential requirement for protecting the central nervous system. Consequently, defining this baseline establishes a critical molecular framework for identifying precise therapeutic targets to combat oxidative stress, excitotoxicity, and age-related neurodegeneration.

Graphical Abstract