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Osteopontin Promotes Left Ventricular Diastolic Dysfunction Through a Mitochondrial Pathway.

Keyvan Yousefi1, Camila I Irion2, Lauro M Takeuchi3

  • 1Department of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida; Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida.

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Summary

Osteopontin (OPN) and OGDHL are key players in chronic kidney disease (CKD) and heart failure with preserved ejection fraction (HFpEF). Targeting OPN and OGDHL may offer new therapeutic strategies for this distinct patient group.

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Alport syndromeHFpEFOGDHLhiPS-CMmitochondriaosteopontin

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Area of Science:

  • Cardiovascular Medicine
  • Nephrology
  • Biochemistry

Background:

  • Heart failure with preserved ejection fraction (HFpEF) in patients with chronic kidney disease (CKD) may represent a unique phenotype.
  • Osteopontin (OPN) is a known biomarker for HFpEF and a predictor of patient outcomes.
  • Previous research showed OPN blockade reversed kidney failure and mitochondrial dysfunction in a mouse model of Alport syndrome.

Purpose of the Study:

  • To identify OPN targets in human heart biopsies and cardiomyocytes.
  • To characterize the cardiac phenotype in Col4a3-/- mice, a model relevant to HFpEF.
  • To investigate the role of OPN in driving cardiomyopathy.

Main Methods:

  • Quantified OGDHL mRNA and protein in myocardial samples from HFpEF patients, heart failure with reduced ejection fraction patients, and controls.
  • Assessed OGDHL expression in human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs) after OPN blockade.
  • Evaluated cardiac parameters in Col4a3-/- mice with and without OPN knockout or Ogdhl gene delivery.

Main Results:

  • OGDHL mRNA and protein levels were significantly altered in HFpEF patient hearts compared to controls.
  • OPN blockade in hiPS-CMs led to increased OGDHL expression.
  • Col4a3-/- mice exhibited HFpEF-like cardiomyopathy, which was improved by OPN deficiency and Ogdhl overexpression, alongside enhanced renal function.

Conclusions:

  • Col4a3-/- mice serve as a valuable model for HFpEF secondary to CKD.
  • OPN and OGDHL are identified as crucial intermediates in this disease model.
  • OPN and OGDHL represent potential therapeutic targets for HFpEF associated with CKD.