Multiscale mitochondrial cristae remodeling links Opa1 downregulation to reduced OXPHOS capacity in aged hearts

I Isidora Molina-Riquelme (Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile) G Gonzalo Barrientos (Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile) L Leonhard Breitsprecher (Center of Cellular Nanoanalytics, Integrated Bioimaging Facility, University of Osnabrück) W Wileidy Gómez (Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile) F Francisco Díaz-Castro (Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile) S Silke Morris (Institute of Integrative Cell Biology and Physiology, Faculty of Biology, University of Muenster) G Gonzalo Almarza (Laboratorio de Fisiología y Bioenergética Celular, Departamento de Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile) A Andrea del Campo (Laboratorio de Fisiología y Bioenergética Celular, Departamento de Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile) L Luis Garrido-Olivares (Laboratorio de Fisiología y Bioenergética Celular, Departamento de Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile) H Hugo E. Verdejo (Facultad de Medicina, División de Cirugía, Pontificia Universidad Católica de Chile) O Olympia Ekaterini Psathaki (Center of Cellular Nanoanalytics, Integrated Bioimaging Facility, University of Osnabrück) K Karin B. Busch (Institute of Integrative Cell Biology and Physiology, Faculty of Biology, University of Muenster) V Verónica Eisner (Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile)

Abstract

Aging is closely associated with cardiovascular diseases, the leading cause of mortality worldwide. Mitochondrial dysfunction is a hallmark of cardiovascular aging. Most of the heart’s ATP is produced at the cristae, specialized subcompartments where oxidative phosphorylation (OXPHOS) takes place. In this study, we used multiple-scale electron microscopy approaches to evaluate age-related mitochondrial and ultrastructural alterations of cristae in human and mouse hearts. We found that aged patients’ hearts displayed reduced cristae density as seen by transmission electron microscopy (TEM), even before any significant decline in the expression of cristae-shaping proteins. Similarly, a multiscale approach that included TEM and serial block-face scanning electron microscopy (SBF-SEM) showed that in aged mice’s hearts, cristae undergo ultrastructural remodeling processes, resulting in a decrease in cristae density and width. Electron tomography suggests an apparent decline in cristae connectivity and an increase in fenestration size. These changes were linked to Opa1 downregulation, accompanied by reduced maximal OXPHOS respiration, but unrelated to alterations in the abundance of OXPHOS core subunits and ATP synthase assembly. Altogether, this indicates that alterations in cristae structure alone are sufficient to impair oxidative metabolism, which highlights its potential as an early signal of cardiac aging, even before noticeable changes in mitochondrial morphology occur.

Article Details

Volume / Issue Vol. 123, Issue 1
Published January 06, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (13)

I

Isidora Molina-Riquelme

Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile

G

Gonzalo Barrientos

Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile

L

Leonhard Breitsprecher

Center of Cellular Nanoanalytics, Integrated Bioimaging Facility, University of Osnabrück

W

Wileidy Gómez

Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile

F

Francisco Díaz-Castro

Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile

S

Silke Morris

Institute of Integrative Cell Biology and Physiology, Faculty of Biology, University of Muenster

G

Gonzalo Almarza

Laboratorio de Fisiología y Bioenergética Celular, Departamento de Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile

A

Andrea del Campo

Laboratorio de Fisiología y Bioenergética Celular, Departamento de Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile

L

Luis Garrido-Olivares

Laboratorio de Fisiología y Bioenergética Celular, Departamento de Farmacia, Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile

H

Hugo E. Verdejo

Facultad de Medicina, División de Cirugía, Pontificia Universidad Católica de Chile

O

Olympia Ekaterini Psathaki

Center of Cellular Nanoanalytics, Integrated Bioimaging Facility, University of Osnabrück

K

Karin B. Busch

Institute of Integrative Cell Biology and Physiology, Faculty of Biology, University of Muenster

V

Verónica Eisner

Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile