Richard N. Kitsis

Albert Einstein College of Medicine — United States

Biochemistry, Genetics and Molecular Biology · Life Sciences

65h-index25.0kcitations198works13.82yr avg
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Research Topics

Cell death mechanisms and regulation(42), Mitochondrial Function and Pathology(37), Autophagy in Disease and Therapy(32), Cardiac Ischemia and Reperfusion(23), PI3K/AKT/mTOR signaling in cancer(18)

Publications195 total

Regulated Cell Death in Myocardial Infarction
Circulation Research·2025· 1 citedOpen Access
Reformulation of the Necroptosis Pathway in Reperfused Myocardial Infarction
Circulation·2025· 2 citedOpen Access
Cell Death in Mouse Kidneys during Cold Ischemia Shows Sexual Dimorphism and Can Be Delayed by a Bax Inhibitor
American Journal of Transplantation·2025
Extracellular Role for the Intracellular Cell Death Mediator RIPK3 in Myocardial Infarction
Circulation·2024· 3 citedOpen Access
OPA1 promotes ferroptosis by augmenting mitochondrial ROS and suppressing an integrated stress response
Molecular Cell·2024· 74 citedOpen Access
Ponatinib-Induced Cardiomyocyte Toxicity: Dark Side of the Integrated Stress Response
Circulation Research·2024· 3 citedOpen Access
The mitochondrial ATP synthase is a negative regulator of the mitochondrial permeability transition pore
Proceedings of the National Academy of Sciences·2023· 26 citedOpen Access
Gasdermin D permeabilization of mitochondrial inner and outer membranes accelerates and enhances pyroptosis
Immunity·2023· 417 citedOpen Access
Priorities in Cardio-Oncology Basic and Translational Science
JACC CardioOncology·2023· 39 citedOpen Access
BAK contributes critically to necrosis and infarct generation during reperfused myocardial infarction
Journal of Molecular and Cellular Cardiology·2023· 4 citedOpen Access
Loss of cyclophilin D prolyl isomerase activity desensitizes mitochondrial permeability transition pore opening in isolated cardiac mitochondria, but does not protect in myocardial ischemia-reperfusion injury
Journal of Molecular and Cellular Cardiology·2023· 4 citedOpen Access
Introduction to review series: Regulated necrosis programs in heart disease
Journal of Molecular and Cellular Cardiology·2023· 1 cited
Supplemental Figure. 4 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Supplemental Figure. 2 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Supplemental Figure.1 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Supplemental Figure. 3 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Data from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Supplemental Figure. 3 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Supplemental Figure. 4 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
Supplemental Figure.1 from An Akt3 Splice Variant Lacking the Serine 472 Phosphorylation Site Promotes Apoptosis and Suppresses Mammary Tumorigenesis
2023Open Access
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Frequent Co-authors

Evripidis Gavathiotis(7), Gerald W. Dorn(7), Madhulika Chandra(6), Stephen M. Factor(6), Jamshid Shirani(6), Wenfeng Miao(5), Kartik Mani(5), Dulguun Amgalan(4), Detlef Wencker(4), Russell S. Whelan(4), Gerald W. Dorn(4), Linda A. Jelicks(4), Peiyee Lee(4), Kenneth Walsh(3), Robert C. Armstrong(3), Young-Jae Nam(3), Klitos Konstantinidis(3), Shani Bialik(3), Herbert B. Tanowitz(3), Michael P. Lisanti(3)