Thomas Krieg

Visiting Scientist

Research Group Home Page:: Brindle Group

Work address:: Cancer Research UK Cambridge Institute University of Cambridge Li Ka Shing Centre Robinson Way Cambridge CB2 0RE

Publications:: Correction to: Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive.

E-pub date: 31 Mar 2019; Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive.

E-pub date: 28 Feb 2019; Selective mitochondrial superoxide generation in vivo is cardioprotective through hormesis.

E-pub date: 31 Jan 2019; Selective Disruption of Mitochondrial Thiol Redox State in Cells and In Vivo.

E-pub date: 30 Nov 2018; Ischemic preconditioning protects against cardiac ischemia reperfusion injury without affecting succinate accumulation or oxidation.

E-pub date: 01 Oct 2018; Mitochondria-derived ROS activate AMP-activated protein kinase (AMPK) indirectly.

E-pub date: 31 Aug 2018; cGMP at the centre of attention: emerging strategies for activating the cardioprotective PKG pathway.

E-pub date: 15 May 2018; Cardioprotection by ischemic postconditioning and cyclic guanosine monophosphate-elevating agents involves cardiomyocyte nitric oxide-sensitive guanylyl cyclase.

E-pub date: 01 May 2018; Metabolomic Profiling in Acute ST-Segment-Elevation Myocardial Infarction Identifies Succinate as an Early Marker of Human Ischemia-Reperfusion Injury.

E-pub date: 06 Apr 2018; Corrigendum to “European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)” [Redox Biol. 13 (2017) 94-162].

E-pub date: 01 Apr 2018; Monoamine oxidase-dependent endoplasmic reticulum-mitochondria dysfunction and mast cell degranulation lead to adverse cardiac remodeling in diabetes.

E-pub date: 19 Feb 2018; cGMP-Elevating Compounds and Ischemic Conditioning Provide Cardioprotection Against Ischemia and Reperfusion Injury via Cardiomyocyte-Specific BK Channels.

E-pub date: 12 Dec 2017; European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).

E-pub date: 31 Oct 2017; MitoNeoD: A Mitochondria-Targeted Superoxide Probe.

E-pub date: 19 Oct 2017; Identification and quantification of protein S-nitrosation by nitrite in the mouse heart during ischemia.

E-pub date: 01 Sep 2017; Assessment of H2S in vivo using the newly developed mitochondria-targeted mass spectrometry probe MitoA.

E-pub date: 12 May 2017; Functional assessment and transplantation of the donor heart after circulatory death.

E-pub date: 31 Dec 2016; Succinate metabolism: a new therapeutic target for myocardial reperfusion injury.

E-pub date: 15 Jul 2016; Moving Forwards by Blocking Back-Flow: The Yin and Yang of MI Therapy.

E-pub date: 04 Mar 2016; Assessing the Mitochondrial Membrane Potential in Cells and In Vivo using Targeted Click Chemistry and Mass Spectrometry.

E-pub date: 09 Feb 2016; A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury.

E-pub date: 09 Feb 2016; Anti-necrotic and cardioprotective effects of a cytosolic renin isoform under ischemia-related conditions.

E-pub date: 31 Jan 2016; Adenosine receptor activation improves microcirculation in experimental intestinal ischemia/reperfusion.

E-pub date: 31 Aug 2015; Combining MRI with PET for partial volume correction improves image-derived input functions in mice.

E-pub date: 01 Jun 2015; Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.

E-pub date: 20 Nov 2014; Trajectory correction for free-breathing radial cine MRI.

E-pub date: 01 Sep 2014; Complex I deficiency due to selective loss of Ndufs4 in the mouse heart results in severe hypertrophic cardiomyopathy.

E-pub date: 31 Aug 2014; Turning on cGMP-dependent pathways to treat cardiac dysfunctions: boom, bust, and beyond.

E-pub date: 31 Aug 2014; Mitochondria selective S-nitrosation by mitochondria-targeted S-nitrosothiol protects against post-infarct heart failure in mouse hearts.

E-pub date: 31 Jul 2014; P439Comparative metabolomics identifies conserved metabolic pathways that control mitochondrial ROS production during ischaemia reperfusion injury.

E-pub date: 15 Jul 2014; Functional assessment of the mouse heart by MRI with a 1-min acquisition.

E-pub date: 01 Jun 2014; A mitochondria-targeted mass spectrometry probe to detect glyoxals: implications for diabetes.

E-pub date: 01 Feb 2014; Using exomarkers to assess mitochondrial reactive species in vivo.

E-pub date: 01 Feb 2014; 6 s-nitrosation of a cysteine switch on mitochondrial complex I protects from acute ischaemia-reperfusion damage and post myocardial infarction heart failure.

E-pub date: 31 Jan 2014; PET/MRI assessment of the infarcted mouse heart.

E-pub date: 31 Dec 2013; MRI and PET in mouse models of myocardial infarction.

E-pub date: 19 Dec 2013; A fast protocol for infarct quantification in mice.

E-pub date: 31 Aug 2013; Riociguat reduces infarct size and post-infarct heart failure in mouse hearts: insights from MRI/PET imaging.

E-pub date: 31 Aug 2013; Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I.

E-pub date: 01 Jun 2013; Protection through postconditioning or a mitochondria-targeted S-nitrosothiol is unaffected by cardiomyocyte-selective ablation of protein kinase G.

E-pub date: 31 Mar 2013; Oxidative and nitrosative stress in the maintenance of myocardial function.

E-pub date: 15 Oct 2012; All preconditioning-related G protein-coupled receptors can be demonstrated in the rabbit cardiomyocyte.

E-pub date: 01 Jun 2012; Evidence for an intracellular localization of the adenosine A2B receptor in rat cardiomyocytes.

E-pub date: 31 May 2011; A2b adenosine receptors in cardioprotection: timing is everything.

E-pub date: 31 Mar 2011; Both A2a and A2b adenosine receptors at reperfusion are necessary to reduce infarct size in mouse hearts.

E-pub date: 31 Oct 2010; Inhibition of glycogen synthase kinase 3beta prevents peroxide-induced collapse of mitochondrial membrane potential in rat ventricular myocytes.

E-pub date: 31 Jul 2010; Cardioprotective effects of mineralocorticoid receptor antagonists at reperfusion.

E-pub date: 31 Jul 2010; AMP579 is revealed to be a potent A2b-adenosine receptor agonist in human 293 cells and rabbit hearts.

E-pub date: 31 Jan 2010; Cardioprotection of bradykinin at reperfusion involves transactivation of the epidermal growth factor receptor via matrix metalloproteinase-8.

E-pub date: 31 Dec 2009; BAY 58-2667, a nitric oxide-independent guanylyl cyclase activator, pharmacologically post-conditions rabbit and rat hearts.

E-pub date: 31 Jul 2009; Prostaglandin receptors mediate effects of substances released from ischaemic rat hearts on non-ischaemic cardiomyocytes.

E-pub date: 31 Dec 2008; Vardenafil protects isolated rat hearts at reperfusion dependent on GC and PKG.

E-pub date: 31 May 2008; Mapping preconditioning’s signaling pathways: an engineering approach.

E-pub date: 31 Mar 2008; Toll-like receptor-4 deficiency attenuates doxorubicin-induced cardiomyopathy in mice.

E-pub date: 31 Mar 2008; The endothelin receptor blocker bosentan inhibits doxorubicin-induced cardiomyopathy.

E-pub date: 01 Nov 2007; COX-2-dependent and potentially cardioprotective effects of negative inotropic substances released after ischemia.

E-pub date: 31 Oct 2007; The delta-opioid receptor agonist DADLE at reperfusion protects the heart through activation of pro-survival kinases via EGF receptor transactivation.

E-pub date: 01 Sep 2007; Preconditioning-mimetics bradykinin and DADLE activate PI3-kinase through divergent pathways.

E-pub date: 01 Apr 2007; Activation of Akt is essential for acetylcholine to trigger generation of oxygen free radicals.

E-pub date: 31 Mar 2003; Show all Hide all

Thomas Krieg

Visiting Scientist

Correction to: Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive.

Protection against cardiac ischemia-reperfusion injury by hypothermia and by inhibition of succinate accumulation and oxidation is additive.

Selective mitochondrial superoxide generation in vivo is cardioprotective through hormesis.

Selective Disruption of Mitochondrial Thiol Redox State in Cells and In Vivo.

Ischemic preconditioning protects against cardiac ischemia reperfusion injury without affecting succinate accumulation or oxidation.

Mitochondria-derived ROS activate AMP-activated protein kinase (AMPK) indirectly.

cGMP at the centre of attention: emerging strategies for activating the cardioprotective PKG pathway.

Cardioprotection by ischemic postconditioning and cyclic guanosine monophosphate-elevating agents involves cardiomyocyte nitric oxide-sensitive guanylyl cyclase.

Metabolomic Profiling in Acute ST-Segment-Elevation Myocardial Infarction Identifies Succinate as an Early Marker of Human Ischemia-Reperfusion Injury.

Corrigendum to “European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)” [Redox Biol. 13 (2017) 94-162].

Monoamine oxidase-dependent endoplasmic reticulum-mitochondria dysfunction and mast cell degranulation lead to adverse cardiac remodeling in diabetes.

cGMP-Elevating Compounds and Ischemic Conditioning Provide Cardioprotection Against Ischemia and Reperfusion Injury via Cardiomyocyte-Specific BK Channels.

European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS).

MitoNeoD: A Mitochondria-Targeted Superoxide Probe.

Identification and quantification of protein S-nitrosation by nitrite in the mouse heart during ischemia.

Assessment of H2S in vivo using the newly developed mitochondria-targeted mass spectrometry probe MitoA.

Functional assessment and transplantation of the donor heart after circulatory death.

Succinate metabolism: a new therapeutic target for myocardial reperfusion injury.

Moving Forwards by Blocking Back-Flow: The Yin and Yang of MI Therapy.

Assessing the Mitochondrial Membrane Potential in Cells and In Vivo using Targeted Click Chemistry and Mass Spectrometry.

A Unifying Mechanism for Mitochondrial Superoxide Production during Ischemia-Reperfusion Injury.

Anti-necrotic and cardioprotective effects of a cytosolic renin isoform under ischemia-related conditions.

Adenosine receptor activation improves microcirculation in experimental intestinal ischemia/reperfusion.

Combining MRI with PET for partial volume correction improves image-derived input functions in mice.

Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.

Trajectory correction for free-breathing radial cine MRI.

Complex I deficiency due to selective loss of Ndufs4 in the mouse heart results in severe hypertrophic cardiomyopathy.

Turning on cGMP-dependent pathways to treat cardiac dysfunctions: boom, bust, and beyond.

Mitochondria selective S-nitrosation by mitochondria-targeted S-nitrosothiol protects against post-infarct heart failure in mouse hearts.

P439Comparative metabolomics identifies conserved metabolic pathways that control mitochondrial ROS production during ischaemia reperfusion injury.

Functional assessment of the mouse heart by MRI with a 1-min acquisition.

A mitochondria-targeted mass spectrometry probe to detect glyoxals: implications for diabetes.

Using exomarkers to assess mitochondrial reactive species in vivo.

6 s-nitrosation of a cysteine switch on mitochondrial complex I protects from acute ischaemia-reperfusion damage and post myocardial infarction heart failure.

PET/MRI assessment of the infarcted mouse heart.

MRI and PET in mouse models of myocardial infarction.

A fast protocol for infarct quantification in mice.

Riociguat reduces infarct size and post-infarct heart failure in mouse hearts: insights from MRI/PET imaging.

Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I.

Protection through postconditioning or a mitochondria-targeted S-nitrosothiol is unaffected by cardiomyocyte-selective ablation of protein kinase G.

Oxidative and nitrosative stress in the maintenance of myocardial function.

All preconditioning-related G protein-coupled receptors can be demonstrated in the rabbit cardiomyocyte.

Evidence for an intracellular localization of the adenosine A2B receptor in rat cardiomyocytes.

A2b adenosine receptors in cardioprotection: timing is everything.

Both A2a and A2b adenosine receptors at reperfusion are necessary to reduce infarct size in mouse hearts.

Inhibition of glycogen synthase kinase 3beta prevents peroxide-induced collapse of mitochondrial membrane potential in rat ventricular myocytes.

Cardioprotective effects of mineralocorticoid receptor antagonists at reperfusion.

AMP579 is revealed to be a potent A2b-adenosine receptor agonist in human 293 cells and rabbit hearts.

Cardioprotection of bradykinin at reperfusion involves transactivation of the epidermal growth factor receptor via matrix metalloproteinase-8.

BAY 58-2667, a nitric oxide-independent guanylyl cyclase activator, pharmacologically post-conditions rabbit and rat hearts.

Prostaglandin receptors mediate effects of substances released from ischaemic rat hearts on non-ischaemic cardiomyocytes.

Vardenafil protects isolated rat hearts at reperfusion dependent on GC and PKG.

Mapping preconditioning’s signaling pathways: an engineering approach.

Toll-like receptor-4 deficiency attenuates doxorubicin-induced cardiomyopathy in mice.

The endothelin receptor blocker bosentan inhibits doxorubicin-induced cardiomyopathy.

COX-2-dependent and potentially cardioprotective effects of negative inotropic substances released after ischemia.

The delta-opioid receptor agonist DADLE at reperfusion protects the heart through activation of pro-survival kinases via EGF receptor transactivation.

Preconditioning-mimetics bradykinin and DADLE activate PI3-kinase through divergent pathways.

Activation of Akt is essential for acetylcholine to trigger generation of oxygen free radicals.

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