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Peer-reviewedCC BY 4.0Frontiers in Molecular Neuroscience

Mechanisms and therapeutic prospects of short-chain fatty acids in neonatal hypoxic–ischemic encephalopathy via modulation of mitochondrial dysfunction and endoplasmic reticulum stress

  • Yinyu Wang1
  • Lingjuan Gao2
  • Yu Xu2
  • Limei Niu1
  • Xuan Tang1
  • Yunxu Zhou3
  • Xianhui Deng1,4
  • Zhidan Bao1
4 affiliations
  1. 1Department of Neonatology, Jiangyin People’s Hospital, Jiangyin, Jiangsu, China
  2. 2Department of Neurosurgery, Jiangyin Clinical College of Xuzhou Medical University, Jiangyin, Jiangsu, China
  3. 3School of Medicine and Health Sciences, Wuxi Taihu University, Wuxi, Jiangsu, China
  4. 4Wuxi Key Laboratory of Biomaterials for Clinical Application, Jiangyin, Jiangsu, China
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Abstract

Neonatal hypoxic–ischemic encephalopathy (HIE) is a common severe neurological disorder following perinatal asphyxia and a leading cause of neonatal mortality and long-term neurodevelopmental impairments, including cerebral palsy, epilepsy, and cognitive and behavioral deficits. It remains one of the primary causes of death and disability in newborns, imposing a substantial burden on families and society. Although therapeutic hypothermia is currently recognized as an effective intervention, its narrow treatment window, limited patient eligibility, and the persistence of significant sequelae in some affected infants underscore the urgent need for adjunctive therapeutic strategies targeting novel mechanisms. In recent years, short-chain fatty acids (SCFAs), which are metabolites of the gut microbiota, have garnered considerable attention due to their neuroprotective effects via the gut–brain axis. This article systematically reviews the potential mechanisms and therapeutic prospects of SCFAs in neonatal HIE, focusing on their modulation of mitochondrial dysfunction and endoplasmic reticulum stress (ERS).

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Cite

BibTeXRIS
BibTeX
@article{wang2026mechanisms,
  title = {{Mechanisms and therapeutic prospects of short-chain fatty acids in neonatal hypoxic–ischemic encephalopathy via modulation of mitochondrial dysfunction and endoplasmic reticulum stress}},
  author = {Yinyu Wang and Lingjuan Gao and Yu Xu and Limei Niu and Xuan Tang and Yunxu Zhou and Xianhui Deng and Zhidan Bao},
  journal = {Frontiers in Molecular Neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnmol.2026.1875196},
  url = {https://doi.org/10.3389/fnmol.2026.1875196},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Mechanisms and therapeutic prospects of short-chain fatty acids in neonatal hypoxic–ischemic encephalopathy via modulation of mitochondrial dysfunction and endoplasmic reticulum stress
AU  - Yinyu Wang
AU  - Lingjuan Gao
AU  - Yu Xu
AU  - Limei Niu
AU  - Xuan Tang
AU  - Yunxu Zhou
AU  - Xianhui Deng
AU  - Zhidan Bao
PY  - 2026
DA  - 2026/10/12
JO  - Frontiers in Molecular Neuroscience
DO  - 10.3389/fnmol.2026.1875196
UR  - https://doi.org/10.3389/fnmol.2026.1875196
AB  - Neonatal hypoxic–ischemic encephalopathy (HIE) is a common severe neurological disorder following perinatal asphyxia and a leading cause of neonatal mortality and long-term neurodevelopmental impairments, including cerebral palsy, epilepsy, and cognitive and behavioral deficits. It remains one of the primary causes of death and disability in newborns, imposing a substantial burden on families and society. Although therapeutic hypothermia is currently recognized as an effective intervention, its narrow treatment window, limited patient eligibility, and the persistence of significant sequelae in some affected infants underscore the urgent need for adjunctive therapeutic strategies targeting novel mechanisms. In recent years, short-chain fatty acids (SCFAs), which are metabolites of the gut microbiota, have garnered considerable attention due to their neuroprotective effects via the gut–brain axis. This article systematically reviews the potential mechanisms and therapeutic prospects of SCFAs in neonatal HIE, focusing on their modulation of mitochondrial dysfunction and endoplasmic reticulum stress (ERS).
SN  - 1662-5099
ER  -