Key result
Cardiac-specific Hsp90β deletion reduces infarct size after ischemia/reperfusion by preserving mitochondrial integrity.
Why the study?
Does cardiac-specific Hsp90β gene ablation improve mitochondrial structure and reduce infarct size after ischemia/reperfusion injury in mice?
Population
Cardiac-specific Hsp90β conditional knockout (cKO) mouse model
Comparison
Cardiac-specific Hsp90β gene ablation vs Control mice
Design
Preclinical
Follow-up
Up to 1 year
Authors
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Cardiac-specific loss of Hsp90β preserves mitochondrial structure under stress and reduces infarct size, suggesting it does not operate as a pro-survival chaperone.
Does cardiac-specific Hsp90β gene ablation improve mitochondrial structure and reduce infarct size after ischemia/reperfusion injury in mice?
Cardiac-specific loss of Hsp90β preserves mitochondrial structure under stress and reduces infarct size, suggesting it does not operate as a pro-survival chaperone.
Roberts et al. (2025) studied Ischemia/reperfusion injury. Cardiac-specific Hsp90β conditional knockout vs. Control was evaluated on Animal survival, heart structure and function, and mitochondrial structure. Cardiac-specific loss of Hsp90β in mice preserved mitochondrial membrane integrity and structure under stress, reducing infarct size after ischemia/reperfusion injury.
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