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  1. Article ; Online: Prolonging Cellular Life after Hypoxic Death.

    Eltzschig, Holger K

    The New England journal of medicine

    2022  Volume 387, Issue 22, Page(s) 2089–2091

    Language English
    Publishing date 2022-11-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr2210456
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  2. Article ; Online: Methylprednisolone for Heart Surgery in Infants.

    Gautam, Nischal K / Salazar, Jorge D / Eltzschig, Holger K

    The New England journal of medicine

    2023  Volume 388, Issue 10, Page(s) 958–959

    MeSH term(s) Infant ; Humans ; Methylprednisolone/therapeutic use ; Cardiac Surgical Procedures ; Postoperative Complications
    Chemical Substances Methylprednisolone (X4W7ZR7023)
    Language English
    Publishing date 2023-03-08
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2300127
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  3. Article ; Online: Hypoxia-stabilized RIPK1 promotes cell death.

    Ruan, Wei / Eltzschig, Holger K / Yuan, Xiaoyi

    Nature cell biology

    2023  Volume 25, Issue 7, Page(s) 921–922

    MeSH term(s) Cell Death ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Apoptosis
    Chemical Substances Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2023-07-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/s41556-023-01176-y
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  4. Article ; Online: Therapeutic targeting of hypoxia inducible factor in acute respiratory distress syndrome.

    Tran, Thu T / Eltzschig, Holger K / Yuan, Xiaoyi

    The Journal of physiology

    2023  

    Abstract: Acute respiratory distress syndrome (ARDS) is characterized by bilateral chest infiltration and acute hypoxic respiratory failure. ARDS carries significant morbidity and mortality despite advancements in medical management, calling for the development of ...

    Abstract Acute respiratory distress syndrome (ARDS) is characterized by bilateral chest infiltration and acute hypoxic respiratory failure. ARDS carries significant morbidity and mortality despite advancements in medical management, calling for the development of novel therapeutic targets. Hypoxia-inducible factor (HIF) is a heterodimeric protein involved in various essential pathways, including metabolic reprogramming, immune modulation, angiogenesis and cell cycle regulation. HIF is routinely degraded in homeostasis conditions via the prolyl hydroxylase domain/von Hippel-Lindau protein pathway. However, HIF is stabilized in ARDS via various mechanisms (oxygen-dependent and independent) as an endogenous protective pathway and plays multifaceted roles in different cell populations. This review focuses on the functional role of HIF and its target genes during ARDS, as well as how HIF has evolved as a therapeutic target in current medical management.
    Language English
    Publishing date 2023-11-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP284599
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  5. Article ; Online: Current Concepts of Mechanical Circulatory Support: Are We Ready to Unload?

    Liang, Yafen / Gregoric, Igor / Kar, Biswajit / Eltzschig, Holger K

    Journal of the American College of Cardiology

    2022  Volume 80, Issue 18, Page(s) e155

    MeSH term(s) Humans ; Heart-Assist Devices ; Extracorporeal Membrane Oxygenation ; Cardiovascular System
    Language English
    Publishing date 2022-10-24
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 605507-2
    ISSN 1558-3597 ; 0735-1097
    ISSN (online) 1558-3597
    ISSN 0735-1097
    DOI 10.1016/j.jacc.2022.04.070
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  6. Article ; Online: Disease Mechanisms of Perioperative Organ Injury.

    Conrad, Catharina / Eltzschig, Holger K

    Anesthesia and analgesia

    2020  Volume 131, Issue 6, Page(s) 1730–1750

    Abstract: Despite substantial advances in anesthesia safety within the past decades, perioperative mortality remains a prevalent problem and can be considered among the top causes of death worldwide. Acute organ failure is a major risk factor of morbidity and ... ...

    Abstract Despite substantial advances in anesthesia safety within the past decades, perioperative mortality remains a prevalent problem and can be considered among the top causes of death worldwide. Acute organ failure is a major risk factor of morbidity and mortality in surgical patients and develops primarily as a consequence of a dysregulated inflammatory response and insufficient tissue perfusion. Neurological dysfunction, myocardial ischemia, acute kidney injury, respiratory failure, intestinal dysfunction, and hepatic impairment are among the most serious complications impacting patient outcome and recovery. Pre-, intra-, and postoperative arrangements, such as enhanced recovery after surgery programs, can contribute to lowering the occurrence of organ dysfunction, and mortality rates have improved with the advent of specialized intensive care units and advances in procedures relating to extracorporeal organ support. However, no specific pharmacological therapies have proven effective in the prevention or reversal of perioperative organ injury. Therefore, understanding the underlying mechanisms of organ dysfunction is essential to identify novel treatment strategies to improve perioperative care and outcomes for surgical patients. This review focuses on recent knowledge of pathophysiological and molecular pathways leading to perioperative organ injury. Additionally, we highlight potential therapeutic targets relevant to the network of events that occur in clinical settings with organ failure.
    MeSH term(s) Acute Kidney Injury/etiology ; Acute Kidney Injury/therapy ; Heart Diseases/etiology ; Heart Diseases/physiopathology ; Heart Diseases/therapy ; Humans ; Liver Diseases/etiology ; Liver Diseases/physiopathology ; Liver Diseases/therapy ; Multiple Organ Failure/etiology ; Multiple Organ Failure/physiopathology ; Multiple Organ Failure/therapy ; Perioperative Care/methods ; Postoperative Complications/etiology ; Postoperative Complications/physiopathology ; Postoperative Complications/therapy ; Risk Factors
    Keywords covid19
    Language English
    Publishing date 2020-12-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80032-6
    ISSN 1526-7598 ; 0003-2999
    ISSN (online) 1526-7598
    ISSN 0003-2999
    DOI 10.1213/ANE.0000000000005191
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    Zs.MO 149: Show issues

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  7. Article: Transcriptional Responses of Different Brain Cell Types to Oxygen Decline.

    Ravel-Godreuil, Camille / Roy, Ethan R / Puttapaka, Srinivas N / Li, Sanming / Wang, Yanyu / Yuan, Xiaoyi / Eltzschig, Holger K / Cao, Wei

    Brain sciences

    2024  Volume 14, Issue 4

    Abstract: Brain hypoxia is associated with a wide range of physiological and clinical conditions. Although oxygen is an essential constituent of maintaining brain functions, our understanding of how specific brain cell types globally respond and adapt to ... ...

    Abstract Brain hypoxia is associated with a wide range of physiological and clinical conditions. Although oxygen is an essential constituent of maintaining brain functions, our understanding of how specific brain cell types globally respond and adapt to decreasing oxygen conditions is incomplete. In this study, we exposed mouse primary neurons, astrocytes, and microglia to normoxia and two hypoxic conditions and obtained genome-wide transcriptional profiles of the treated cells. Analysis of differentially expressed genes under conditions of reduced oxygen revealed a canonical hypoxic response shared among different brain cell types. In addition, we observed a higher sensitivity of neurons to oxygen decline, and dissected cell type-specific biological processes affected by hypoxia. Importantly, this study establishes novel gene modules associated with brain cells responding to oxygen deprivation and reveals a state of profound stress incurred by hypoxia.
    Language English
    Publishing date 2024-03-30
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2651993-8
    ISSN 2076-3425
    ISSN 2076-3425
    DOI 10.3390/brainsci14040341
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  8. Article ; Online: Targeting hypoxia-inducible factors: therapeutic opportunities and challenges.

    Yuan, Xiaoyi / Ruan, Wei / Bobrow, Bentley / Carmeliet, Peter / Eltzschig, Holger K

    Nature reviews. Drug discovery

    2023  Volume 23, Issue 3, Page(s) 175–200

    Abstract: Hypoxia-inducible factors (HIFs) are highly conserved transcription factors that are crucial for adaptation of metazoans to limited oxygen availability. Recently, HIF activation and inhibition have emerged as therapeutic targets in various human diseases. ...

    Abstract Hypoxia-inducible factors (HIFs) are highly conserved transcription factors that are crucial for adaptation of metazoans to limited oxygen availability. Recently, HIF activation and inhibition have emerged as therapeutic targets in various human diseases. Pharmacologically desirable effects of HIF activation include erythropoiesis stimulation, cellular metabolism optimization during hypoxia and adaptive responses during ischaemia and inflammation. By contrast, HIF inhibition has been explored as a therapy for various cancers, retinal neovascularization and pulmonary hypertension. This Review discusses the biochemical mechanisms that control HIF stabilization and the molecular strategies that can be exploited pharmacologically to activate or inhibit HIFs. In addition, we examine medical conditions that benefit from targeting HIFs, the potential side effects of HIF activation or inhibition and future challenges in this field.
    MeSH term(s) Humans ; Basic Helix-Loop-Helix Transcription Factors ; Hypoxia/drug therapy ; Hypoxia/metabolism ; Transcription Factors ; Neoplasms/drug therapy ; Oxygen
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; Transcription Factors ; Oxygen (S88TT14065)
    Language English
    Publishing date 2023-12-20
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2062954-0
    ISSN 1474-1784 ; 1474-1776
    ISSN (online) 1474-1784
    ISSN 1474-1776
    DOI 10.1038/s41573-023-00848-6
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  9. Article ; Online: Interplay of hypoxia-inducible factors and oxygen therapy in cardiovascular medicine.

    Liang, Yafen / Ruan, Wei / Jiang, Yandong / Smalling, Richard / Yuan, Xiaoyi / Eltzschig, Holger K

    Nature reviews. Cardiology

    2023  Volume 20, Issue 11, Page(s) 723–737

    Abstract: Mammals have evolved to adapt to differences in oxygen availability. Although systemic oxygen homeostasis relies on respiratory and circulatory responses, cellular adaptation to hypoxia involves the transcription factor hypoxia-inducible factor (HIF). ... ...

    Abstract Mammals have evolved to adapt to differences in oxygen availability. Although systemic oxygen homeostasis relies on respiratory and circulatory responses, cellular adaptation to hypoxia involves the transcription factor hypoxia-inducible factor (HIF). Given that many cardiovascular diseases involve some degree of systemic or local tissue hypoxia, oxygen therapy has been used liberally over many decades for the treatment of cardiovascular disorders. However, preclinical research has revealed the detrimental effects of excessive use of oxygen therapy, including the generation of toxic oxygen radicals or attenuation of endogenous protection by HIFs. In addition, investigators in clinical trials conducted in the past decade have questioned the excessive use of oxygen therapy and have identified specific cardiovascular diseases in which a more conservative approach to oxygen therapy could be beneficial compared with a more liberal approach. In this Review, we provide numerous perspectives on systemic and molecular oxygen homeostasis and the pathophysiological consequences of excessive oxygen use. In addition, we provide an overview of findings from clinical studies on oxygen therapy for myocardial ischaemia, cardiac arrest, heart failure and cardiac surgery. These clinical studies have prompted a shift from liberal oxygen supplementation to a more conservative and vigilant approach to oxygen therapy. Furthermore, we discuss the alternative therapeutic strategies that target oxygen-sensing pathways, including various preconditioning approaches and pharmacological HIF activators, that can be used regardless of the level of oxygen therapy that a patient is already receiving.
    MeSH term(s) Animals ; Humans ; Cardiovascular Diseases/drug therapy ; Hypoxia/therapy ; Oxygen/therapeutic use ; Oxygen/metabolism ; Oxygen Inhalation Therapy ; Gene Expression Regulation ; Mammals/metabolism
    Chemical Substances Oxygen (S88TT14065)
    Language English
    Publishing date 2023-06-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/s41569-023-00886-y
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  10. Article ; Online: Targeting the Hypoxia-Adenosine Link for Controlling Excessive Inflammation.

    Czopik, Agnieszka / Yuan, Xiaoyi / Evans, Scott E / Eltzschig, Holger K

    Anesthesiology

    2021  Volume 135, Issue 1, Page(s) 15–17

    MeSH term(s) Humans ; Adenosine ; Hypoxia ; Inflammation
    Chemical Substances Adenosine (K72T3FS567)
    Language English
    Publishing date 2021-02-22
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 269-0
    ISSN 1528-1175 ; 0003-3022
    ISSN (online) 1528-1175
    ISSN 0003-3022
    DOI 10.1097/ALN.0000000000003841
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