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Peer-reviewedCC BY 4.0Frontiers in Pharmacology

Natural polysaccharides as modulators of mitochondrial homeostasis: structural determinants, pharmacological mechanisms, and translational challenges

  • Xinfang Du1,2
  • Jingwen Zhang1,2
  • Wenjing Li1,2
  • Qinying Li1,2
  1. 1Clinical Research Center, Affiliated Hospital of Shandong Second Medical University
  2. 2Department of Endocrinology and Metabolism, Affiliated Hospital of Shandong Second Medical University
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Abstract

Mitochondrial dysfunction is a convergent pathological feature of neurodegenerative, metabolic, cardiovascular, hepatic, and cancer-related disorders, making mitochondrial homeostasis an important therapeutic target. Natural polysaccharides (NPs) are structurally diverse macromolecules that have emerged as promising multifunctional modulators of mitochondrial homeostasis. This review summarizes the structural basis and mechanistic actions underlying the mitochondrial regulatory effects of NPs. Key structural features, including molecular weight, monosaccharide composition, glycosidic linkages, branching patterns, and chemical modifications, largely determine the mitochondria-regulating potential of NPs. Mechanistically, NPs regulate mitochondrial homeostasis by restoring bioenergetic function, reducing oxidative stress, maintaining mitochondrial quality control, and modulating mitochondria-dependent apoptosis. These effects support disease-context-specific therapeutic benefits, as NPs generally preserve mitochondrial homeostasis in non-malignant diseases while potentially inducing mitochondrial stress and cell death in cancer. This review also highlights key translational barriers to NP-based mitochondrial therapy, underscoring the need for standardized structural characterization, mechanism-oriented mitochondrial assays, and disease-specific evaluation.

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Cite

BibTeXRIS
BibTeX
@article{du2026natural,
  title = {{Natural polysaccharides as modulators of mitochondrial homeostasis: structural determinants, pharmacological mechanisms, and translational challenges}},
  author = {Xinfang Du and Jingwen Zhang and Wenjing Li and Qinying Li},
  journal = {Frontiers in Pharmacology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphar.2026.1948381},
  url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1948381/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Natural polysaccharides as modulators of mitochondrial homeostasis: structural determinants, pharmacological mechanisms, and translational challenges
AU  - Xinfang Du
AU  - Jingwen Zhang
AU  - Wenjing Li
AU  - Qinying Li
PY  - 2026
DA  - 2026/10/14
JO  - Frontiers in Pharmacology
DO  - 10.3389/fphar.2026.1948381
UR  - https://www.frontiersin.org/articles/10.3389/fphar.2026.1948381/full
AB  - Mitochondrial dysfunction is a convergent pathological feature of neurodegenerative, metabolic, cardiovascular, hepatic, and cancer-related disorders, making mitochondrial homeostasis an important therapeutic target. Natural polysaccharides (NPs) are structurally diverse macromolecules that have emerged as promising multifunctional modulators of mitochondrial homeostasis. This review summarizes the structural basis and mechanistic actions underlying the mitochondrial regulatory effects of NPs. Key structural features, including molecular weight, monosaccharide composition, glycosidic linkages, branching patterns, and chemical modifications, largely determine the mitochondria-regulating potential of NPs. Mechanistically, NPs regulate mitochondrial homeostasis by restoring bioenergetic function, reducing oxidative stress, maintaining mitochondrial quality control, and modulating mitochondria-dependent apoptosis. These effects support disease-context-specific therapeutic benefits, as NPs generally preserve mitochondrial homeostasis in non-malignant diseases while potentially inducing mitochondrial stress and cell death in cancer. This review also highlights key translational barriers to NP-based mitochondrial therapy, underscoring the need for standardized structural characterization, mechanism-oriented mitochondrial assays, and disease-specific evaluation.
SN  - 1663-9812
ER  -