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Related Concept Videos

Mitochondrial Precursor Proteins01:39

Mitochondrial Precursor Proteins

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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
Most of the mitochondrial...
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Translocation of Proteins into the Mitochondria01:19

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
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Related Experiment Video

Updated: Feb 16, 2026

Measuring Mitochondrial Electron Transfer Complexes in Previously Frozen Cardiac Tissue from the Offspring of Sow: A Model to Assess Exercise-Induced Mitochondrial Bioenergetics Changes
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Mitochondrial targeted peptides preserve mitochondrial organization and decrease reversible myocardial changes in

Fang Yuan1,2, John R Woollard1, Kyra L Jordan1

  • 1Department of Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.

Cardiovascular Research
|December 22, 2017
PubMed
Summary

Early metabolic syndrome (MetS) causes reversible cardiac damage by disrupting the cardiomyocyte cytoskeletal-mitochondria-SR network. Treatment with elamipretide (ELAM) improved mitochondrial function and attenuated damage, suggesting new therapeutic targets.

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Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Metabolic Syndrome Research

Background:

  • Early metabolic syndrome (MetS) is linked to cardiac damage, but the underlying mechanisms are unclear.
  • Mitochondria, cytoskeleton, and sarcoplasmic reticulum (SR) interactions are crucial for cardiac function.
  • Altered cytoskeletal-mitochondria-SR interaction is hypothesized to contribute to early MetS cardiac damage.

Purpose of the Study:

  • To investigate the role of cytoskeletal-mitochondria-SR interaction in early MetS-induced cardiac damage.
  • To determine if mitochondrial dysfunction is a key feature of early MetS in the heart.
  • To evaluate the therapeutic potential of elamipretide (ELAM) in mitigating MetS-related cardiac changes.

Main Methods:

  • Diet-induced MetS in domestic pigs for 16 weeks, with some treated with elamipretide (ELAM) for the final 4 weeks.
  • Assessment of cardiac remodeling and function using fast-computed tomography.
  • Ex-vivo analysis of myocardial mitochondrial structure, SR-mitochondria interaction, calcium handling, cytoskeletal proteins, oxidative stress, and apoptosis.

Main Results:

  • MetS pigs exhibited hyperlipidemia, hypertension, and insulin resistance, but preserved cardiac function.
  • MetS induced mitochondrial disorganization, altered cardiolipin, disrupted ATP/ADP balance, decreased cytochrome-c oxidase (COX)-IV activity, increased oxidative stress, and apoptosis.
  • Elamipretide (ELAM) treatment improved mitochondrial organization, restored metabolic balance, reduced oxidative stress and apoptosis, and enhanced SR-mitochondria interaction.

Conclusions:

  • Disorganization of the cardiomyocyte cytoskeletal-mitochondria-SR network is associated with reversible cardiac changes in early MetS.
  • These early, pre-dysfunction cardiac alterations highlight novel therapeutic targets for mitigating MetS-related heart damage.