Thomas Jefferson University
Sidney Kimmel Medical College
Department of Medicine

Gomez, Ludovic

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Ludovic Gomez, PhD

Ludovic Gomez, PhD

Contact Dr. Gomez

1020 Locust Street
Room 533
Philadelphia, PA 19107

(215) 503-0445
(215) 955-1690 fax

Medical School

PhD Claude Bernard Lyon1 University, France 2006

Board Certification

PhD Claude Bernard Lyon1 University, France

University Appointment

Assistant Professor at INSERM (2012)
Visiting Assistant Professor at TJU (2013)

Research & Clinical Interests

Coronary heart disease is the leading cause of death in western countries. Myocardial infarction is a disabling disease, with infarct size being a major determinant of mortality after this common acute coronary event. Myocardial conditioning is an endogenous cardioprotective phenomenon that profoundly limits infarct size in experimental models. Currently, our challenge is to understand protection mechanisms and to translate this paradigm from the laboratory to the clinic, with the ultimate aim of limiting the burden of ischemic heart disease and potentially providing protection for other organs at risk of reperfusion injury, such as brain and kidney.

Key words: Permeability transition pore; calcium signaling; calcium mobilization from sarco/endoplasmic reticulum to mitochondria;  cell death and cardioprotection.


Most Recent Peer-Reviewed Publications

  1. Disruption of calcium transfer from ER to mitochondria links alterations of mitochondria-associated ER membrane integrity to hepatic insulin resistance
  2. The SR/ER-mitochondria calcium crosstalk is regulated by GSK3β during reperfusion injury
  3. Erratum : The SR/ER-mitochondria calcium crosstalk is regulated by GSK3β during reperfusion injury (Cell Death and Differentiation (2015) 22:1890)
  4. Depressing mitochondria-reticulum interactions protects cardiomyocytes from lethal hypoxia-reoxygenation injury
  5. Opposite and tissue-specific effects of coenzyme Q 2 on mPTP opening and ROS production between heart and liver mitochondria: Role of complex I
  6. Postconditioning modulates ischemia-damaged mitochondria during reperfusion
  7. Activation of mitochondrial μ-calpain increases AIF cleavage in cardiac mitochondria during ischemia-reperfusion
  8. A novel role for mitochondrial sphingosine-1-phosphate produced by sphingosine kinase-2 in PTP-mediated cell survival during cardioprotection
  9. Strain-rate imaging predicts the attenuation of left ventricular remodeling induced by Ischemic postconditioning after myocardial infarction in mice
  10. Postconditioning: From the bench to bedside
  11. Sphingosine-1-phosphate produced by sphingosine kinase 2 in mitochondria interacts with prohibitin 2 to regulate complex IV assembly and respiration
  12. Second-generation sulfonylureas preserve inhibition of mitochondrial permeability transition by the mitochondrial K + ATP opener nicorandil in experimental myocardial infarction
  13. Inhibition of mitochondrial permeability transition pore opening: Translation to patients
  14. Heart lesions associated with anabolic steroid abuse: Comparison of post-mortem findings in athletes and norethandrolone-induced lesions in rabbits
  15. Postconditioning inhibits mPTP opening independent of oxidative phosphorylation and membrane potential
  16. Regional Myocardial Function After Myocardial Infarction in Mice: A Follow-Up Study by Strain Rate Imaging
  17. Persistent inhibition of mitochondrial permeability transition by preconditioning during the first hours of reperfusion
  18. Inhibition of GSK3β by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion
  19. Increased mitochondrial calcium coexists with decreased reperfusion injury in postconditioned (but not preconditioned) hearts
  20. Inhibition of mitochondrial permeability transition improves functional recovery and reduces mortality following acute myocardial infarction in mice