Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 52 min ago
Peer-reviewedCC BYAnnals of the New York Academy of Sciences

Respirasome Persistence Without Efficient Electron Channeling in Cardiac Mitochondria From an Animal Model of Hypertension

  • Patrycja Anna Glogowski1
  • Cristina Algieri2
  • Antonia Cugliari3
  • Maria Cotugno4
  • Fabiana Trombetti3
  • Micaela Fabbri3
  • Arrigo Francesco Giuseppe Cicero1
  • Speranza Rubattu4
  • Salvatore Nesci3
4 affiliations
  1. 1IRCCS Azienda Ospedaliero‐Universitaria di Bologna
  2. 2Link University
  3. 3University of Bologna
  4. 4IRCCS Neuromed
Read full textPDFDOICite

Abstract

Cardiac mitochondrial dysfunction contributes to hypertensive remodeling, but whether respiratory supercomplex organization preserves electron transfer efficiency during disease progression remains unresolved. Here, we examined the structural and functional organization of the respiratory complexes in cardiac mitochondria from stroke-resistant and stroke-prone spontaneously hypertensive rats exposed to normal or Japanese diet regimens. In both models, supramolecular analyses revealed the persistence of N-respirasome and Q-respirasome assemblies, indicating that major respiratory supercomplex species are maintained during sustained hypertension and in the pre-stroke state. However, metabolic flux control analysis consistently showed that cytochrome c oxidase or Complex IV exerted only limited control over respiratory flux, with control coefficients below those expected for tightly channeled nicotinamide adenine dinucleotide (NADH)-dependent electron transfer. Thus, structural preservation of respirasomes was not matched by evidence of kinetically optimized coupling. These findings uncouple supercomplex detectability from functional electron channeling and suggest that, in the hypertensive heart, respiratory performance is constrained by qualitative defects in supercomplex organization rather than by their overt loss.

Related

  1. Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity
    Temitayo T. Bamgbose, Oluwakemi Osarumwense Igiehon, Javier Nión Fieira +3
    Frontiers in ImmunologyPeer-reviewedCC BYFull text6 citedEnzymology & metabolismOpenAlex
  2. Isoprenoid Binding and Substrate Channeling in Drimenol Synthase, a Bifunctional Class II Terpene Cyclase-Phosphatase
    K. R. Osika, M. E. Leffler, B. A. R. Czarnecki +1
    bioRxivPreprintCC BY-NC-NDFull textMolecular biology & gene regulationbioRxiv
  3. A quantum state of mitochondria in the living cell
    Y. Yang, Z. Gu, B. Song
    bioRxivPreprintAll rights reservedFull textBiophysicsbioRxiv
  4. Mitochondria poor but capacity rich? The paradox of podocyte respiration
    Antonio S. Novaes, Ilse S. Daehn
    Kidney internationalPeer-reviewedLicence not statedFull textMolecular biology & gene regulationPMC
  5. Pathogenesis of Calcium Oxalate Kidney Stones, Interactions Among Mitochondria, NADPH Oxidase and Endoplasmic Reticulum
    Saeed R. Khan, Abdel A. Alli
    BiomoleculesPeer-reviewedCC BYFull textGeneral biochemistryEurope PMC

Cite

BibTeXRIS
BibTeX
@article{glogowski2026respirasome,
  title = {{Respirasome Persistence Without Efficient Electron Channeling in Cardiac Mitochondria From an Animal Model of Hypertension}},
  author = {Patrycja Anna Glogowski and Cristina Algieri and Antonia Cugliari and Maria Cotugno and Fabiana Trombetti and Micaela Fabbri and Arrigo Francesco Giuseppe Cicero and Speranza Rubattu and Salvatore Nesci},
  journal = {Annals of the New York Academy of Sciences},
  year = {2026},
  month = oct,
  doi = {10.1111/nyas.70440},
  url = {https://europepmc.org/article/PMC/PMC13722159},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Respirasome Persistence Without Efficient Electron Channeling in Cardiac Mitochondria From an Animal Model of Hypertension
AU  - Patrycja Anna Glogowski
AU  - Cristina Algieri
AU  - Antonia Cugliari
AU  - Maria Cotugno
AU  - Fabiana Trombetti
AU  - Micaela Fabbri
AU  - Arrigo Francesco Giuseppe Cicero
AU  - Speranza Rubattu
AU  - Salvatore Nesci
PY  - 2026
DA  - 2026/10/30
JO  - Annals of the New York Academy of Sciences
DO  - 10.1111/nyas.70440
UR  - https://europepmc.org/article/PMC/PMC13722159
AB  - Cardiac mitochondrial dysfunction contributes to hypertensive remodeling, but whether respiratory supercomplex organization preserves electron transfer efficiency during disease progression remains unresolved. Here, we examined the structural and functional organization of the respiratory complexes in cardiac mitochondria from stroke-resistant and stroke-prone spontaneously hypertensive rats exposed to normal or Japanese diet regimens. In both models, supramolecular analyses revealed the persistence of N-respirasome and Q-respirasome assemblies, indicating that major respiratory supercomplex species are maintained during sustained hypertension and in the pre-stroke state. However, metabolic flux control analysis consistently showed that cytochrome c oxidase or Complex IV exerted only limited control over respiratory flux, with control coefficients below those expected for tightly channeled nicotinamide adenine dinucleotide (NADH)-dependent electron transfer. Thus, structural preservation of respirasomes was not matched by evidence of kinetically optimized coupling. These findings uncouple supercomplex detectability from functional electron channeling and suggest that, in the hypertensive heart, respiratory performance is constrained by qualitative defects in supercomplex organization rather than by their overt loss.
SN  - 0077-8923
SN  - 1749-6632
ER  -