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Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation.

Basic research in cardiology

Chang Y, Li X, Cheng Q, Hu Y, Chen X, Hua X, Fan X, Tao M, Song J, Hu S.
PMID: 34870762
Basic Res Cardiol. 2021 Dec 06;116(1):64. doi: 10.1007/s00395-021-00904-5.

Acute rejection (AR) is an important contributor to graft failure, which remains a leading cause of death after heart transplantation (HTX). The regulation of immune metabolism has become a new hotspot in the development of immunosuppressive drugs. In this...

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Chang Y, Li X, Cheng Q, et al. Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation. Basic Res Cardiol. 2021;116(1):64doi: 10.1007/s00395-021-00904-5.
Chang, Y., Li, X., Cheng, Q., Hu, Y., Chen, X., Hua, X., Fan, X., Tao, M., Song, J., & Hu, S. (2021). Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation. Basic research in cardiology, 116(1), 64. https://doi.org/10.1007/s00395-021-00904-5
Chang, Yuan, et al. "Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation." Basic research in cardiology vol. 116,1 (2021): 64. doi: https://doi.org/10.1007/s00395-021-00904-5
Chang Y, Li X, Cheng Q, Hu Y, Chen X, Hua X, Fan X, Tao M, Song J, Hu S. Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation. Basic Res Cardiol. 2021 Dec 06;116(1):64. doi: 10.1007/s00395-021-00904-5. PMID: 34870762.
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Cardioprotection by remote ischemic conditioning is transferable by plasma and mediated by extracellular vesicles.

Basic research in cardiology

Lassen TR, Just J, Hjortbak MV, Jespersen NR, Stenz KT, Gu T, Yan Y, Su J, Hansen J, Bæk R, Jørgensen MM, Nyengaard JR, Kristiansen SB, Drasbek KR, Kjems J, Bøtker HE.
PMID: 33689033
Basic Res Cardiol. 2021 Mar 10;116(1):16. doi: 10.1007/s00395-021-00856-w.

BACKGROUND: Remote ischemic conditioning (RIC) by brief periods of limb ischemia and reperfusion protects against ischemia-reperfusion injury. We studied the cardioprotective role of extracellular vesicles (EV)s released into the circulation after RIC and EV accumulation in injured myocardium.METHODS: We...

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Lassen TR, Just J, Hjortbak MV, et al. Cardioprotection by remote ischemic conditioning is transferable by plasma and mediated by extracellular vesicles. Basic Res Cardiol. 2021;116(1):16doi: 10.1007/s00395-021-00856-w.
Lassen, T. R., Just, J., Hjortbak, M. V., Jespersen, N. R., Stenz, K. T., Gu, T., Yan, Y., Su, J., Hansen, J., Bæk, R., Jørgensen, M. M., Nyengaard, J. R., Kristiansen, S. B., Drasbek, K. R., Kjems, J., & Bøtker, H. E. (2021). Cardioprotection by remote ischemic conditioning is transferable by plasma and mediated by extracellular vesicles. Basic research in cardiology, 116(1), 16. https://doi.org/10.1007/s00395-021-00856-w
Lassen, Thomas Ravn, et al. "Cardioprotection by remote ischemic conditioning is transferable by plasma and mediated by extracellular vesicles." Basic research in cardiology vol. 116,1 (2021): 16. doi: https://doi.org/10.1007/s00395-021-00856-w
Lassen TR, Just J, Hjortbak MV, Jespersen NR, Stenz KT, Gu T, Yan Y, Su J, Hansen J, Bæk R, Jørgensen MM, Nyengaard JR, Kristiansen SB, Drasbek KR, Kjems J, Bøtker HE. Cardioprotection by remote ischemic conditioning is transferable by plasma and mediated by extracellular vesicles. Basic Res Cardiol. 2021 Mar 10;116(1):16. doi: 10.1007/s00395-021-00856-w. PMID: 33689033.
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The zinc transporter ZIP7 (Slc39a7) controls myocardial reperfusion injury by regulating mitophagy.

Basic research in cardiology

Zhang H, Yang N, He H, Chai J, Cheng X, Zhao H, Zhou D, Teng T, Kong X, Yang Q, Xu Z.
PMID: 34581906
Basic Res Cardiol. 2021 Sep 28;116(1):54. doi: 10.1007/s00395-021-00894-4.

Whereas elimination of damaged mitochondria by mitophagy is proposed to be cardioprotective, the regulation of mitophagy at reperfusion and the underlying mechanism remain elusive. Since mitochondrial Zn

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Zhang H, Yang N, He H, et al. The zinc transporter ZIP7 (Slc39a7) controls myocardial reperfusion injury by regulating mitophagy. Basic Res Cardiol. 2021;116(1):54doi: 10.1007/s00395-021-00894-4.
Zhang, H., Yang, N., He, H., Chai, J., Cheng, X., Zhao, H., Zhou, D., Teng, T., Kong, X., Yang, Q., & Xu, Z. (2021). The zinc transporter ZIP7 (Slc39a7) controls myocardial reperfusion injury by regulating mitophagy. Basic research in cardiology, 116(1), 54. https://doi.org/10.1007/s00395-021-00894-4
Zhang, Hualu, et al. "The zinc transporter ZIP7 (Slc39a7) controls myocardial reperfusion injury by regulating mitophagy." Basic research in cardiology vol. 116,1 (2021): 54. doi: https://doi.org/10.1007/s00395-021-00894-4
Zhang H, Yang N, He H, Chai J, Cheng X, Zhao H, Zhou D, Teng T, Kong X, Yang Q, Xu Z. The zinc transporter ZIP7 (Slc39a7) controls myocardial reperfusion injury by regulating mitophagy. Basic Res Cardiol. 2021 Sep 28;116(1):54. doi: 10.1007/s00395-021-00894-4. PMID: 34581906.
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Beyond maximizing: some remarks on optimality and efficiency in the social sciences.

Basic research in cardiology

Acham K.
PMID: 8147831
Basic Res Cardiol. 1993;88:147-57.

The author is dealing with the concept of homo oeconomicus and its relationships to maximizing, satisficing and optimizing practices, from the viewpoint of social sciences. Whereas in physics extremality-principles hold sway, in human affairs the "best" goals and courses...

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Acham K. Beyond maximizing: some remarks on optimality and efficiency in the social sciences. Basic Res Cardiol. 1993;88:147-57
Acham, K. (1993). Beyond maximizing: some remarks on optimality and efficiency in the social sciences. Basic research in cardiology, 88147-57.
Acham, K. "Beyond maximizing: some remarks on optimality and efficiency in the social sciences." Basic research in cardiology vol. 88 (1993): 147-57.
Acham K. Beyond maximizing: some remarks on optimality and efficiency in the social sciences. Basic Res Cardiol. 1993;88:147-57. PMID: 8147831.
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Retraction Note to: Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats.

Basic research in cardiology

Wang ZF, Wang NP, Harmouche S, Philip T, Pang XF, Bai F, Zhao ZQ.
PMID: 25672668
Basic Res Cardiol. 2015 Mar;110(2):12. doi: 10.1007/s00395-015-0469-6.

No abstract available.

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Wang ZF, Wang NP, Harmouche S, et al. Retraction Note to: Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats. Basic Res Cardiol. 2015;110(2):12doi: 10.1007/s00395-015-0469-6.
Wang, Z. F., Wang, N. P., Harmouche, S., Philip, T., Pang, X. F., Bai, F., & Zhao, Z. Q. (2015). Retraction Note to: Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats. Basic research in cardiology, 110(2), 12. https://doi.org/10.1007/s00395-015-0469-6
Wang, Zhang-Feng, et al. "Retraction Note to: Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats." Basic research in cardiology vol. 110,2 (2015): 12. doi: https://doi.org/10.1007/s00395-015-0469-6
Wang ZF, Wang NP, Harmouche S, Philip T, Pang XF, Bai F, Zhao ZQ. Retraction Note to: Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats. Basic Res Cardiol. 2015 Mar;110(2):12. doi: 10.1007/s00395-015-0469-6. PMID: 25672668.
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Preclinical trial of a MAP4K4 inhibitor to reduce infarct size in the pig: does cardioprotection in human stem cell-derived myocytes predict success in large mammals?.

Basic research in cardiology

Te Lintel Hekkert M, Newton G, Chapman K, Aqil R, Downham R, Yan R, Merkus D, Whitlock G, Lane CAL, Cawkill D, Perrior T, Duncker DJ, Schneider MD.
PMID: 34018053
Basic Res Cardiol. 2021 May 20;116(1):34. doi: 10.1007/s00395-021-00875-7.

Reducing infarct size (IS) by interfering with mechanisms for cardiomyocyte death remains an elusive goal. DMX-5804, a selective inhibitor of the stress-activated kinase MAP4K4, suppresses cell death in mouse myocardial infarction (MI), human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs), and...

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Te Lintel Hekkert M, Newton G, Chapman K, et al. Preclinical trial of a MAP4K4 inhibitor to reduce infarct size in the pig: does cardioprotection in human stem cell-derived myocytes predict success in large mammals?. Basic Res Cardiol. 2021;116(1):34doi: 10.1007/s00395-021-00875-7.
Te Lintel Hekkert, M., Newton, G., Chapman, K., Aqil, R., Downham, R., Yan, R., Merkus, D., Whitlock, G., Lane, C. A. L., Cawkill, D., Perrior, T., Duncker, D. J., & Schneider, M. D. (2021). Preclinical trial of a MAP4K4 inhibitor to reduce infarct size in the pig: does cardioprotection in human stem cell-derived myocytes predict success in large mammals?. Basic research in cardiology, 116(1), 34. https://doi.org/10.1007/s00395-021-00875-7
Te Lintel Hekkert, Maaike, et al. "Preclinical trial of a MAP4K4 inhibitor to reduce infarct size in the pig: does cardioprotection in human stem cell-derived myocytes predict success in large mammals?." Basic research in cardiology vol. 116,1 (2021): 34. doi: https://doi.org/10.1007/s00395-021-00875-7
Te Lintel Hekkert M, Newton G, Chapman K, Aqil R, Downham R, Yan R, Merkus D, Whitlock G, Lane CAL, Cawkill D, Perrior T, Duncker DJ, Schneider MD. Preclinical trial of a MAP4K4 inhibitor to reduce infarct size in the pig: does cardioprotection in human stem cell-derived myocytes predict success in large mammals?. Basic Res Cardiol. 2021 May 20;116(1):34. doi: 10.1007/s00395-021-00875-7. PMID: 34018053; PMCID: PMC8137473.
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Protective effect of HINT2 on mitochondrial function via repressing MCU complex activation attenuates cardiac microvascular ischemia-reperfusion injury.

Basic research in cardiology

Li S, Chen J, Liu M, Chen Y, Wu Y, Li Q, Ma T, Gao J, Xia Y, Fan M, Chen A, Lu D, Su E, Xu F, Chen Z, Qian J, Ge J.
PMID: 34914018
Basic Res Cardiol. 2021 Dec 16;116(1):65. doi: 10.1007/s00395-021-00905-4.

Current evidence indicates that coronary microcirculation is a key target for protecting against cardiac ischemia-reperfusion (I/R) injury. Mitochondrial calcium uniporter (MCU) complex activation and mitochondrial calcium ([Ca

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Li S, Chen J, Liu M, et al. Protective effect of HINT2 on mitochondrial function via repressing MCU complex activation attenuates cardiac microvascular ischemia-reperfusion injury. Basic Res Cardiol. 2021;116(1):65doi: 10.1007/s00395-021-00905-4.
Li, S., Chen, J., Liu, M., Chen, Y., Wu, Y., Li, Q., Ma, T., Gao, J., Xia, Y., Fan, M., Chen, A., Lu, D., Su, E., Xu, F., Chen, Z., Qian, J., & Ge, J. (2021). Protective effect of HINT2 on mitochondrial function via repressing MCU complex activation attenuates cardiac microvascular ischemia-reperfusion injury. Basic research in cardiology, 116(1), 65. https://doi.org/10.1007/s00395-021-00905-4
Li, Su, et al. "Protective effect of HINT2 on mitochondrial function via repressing MCU complex activation attenuates cardiac microvascular ischemia-reperfusion injury." Basic research in cardiology vol. 116,1 (2021): 65. doi: https://doi.org/10.1007/s00395-021-00905-4
Li S, Chen J, Liu M, Chen Y, Wu Y, Li Q, Ma T, Gao J, Xia Y, Fan M, Chen A, Lu D, Su E, Xu F, Chen Z, Qian J, Ge J. Protective effect of HINT2 on mitochondrial function via repressing MCU complex activation attenuates cardiac microvascular ischemia-reperfusion injury. Basic Res Cardiol. 2021 Dec 16;116(1):65. doi: 10.1007/s00395-021-00905-4. PMID: 34914018.
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Mitochondrial DNA integrity and function are critical for endothelium-dependent vasodilation in rats with metabolic syndrome.

Basic research in cardiology

Kiyooka T, Ohanyan V, Yin L, Pung YF, Chen YR, Chen CL, Kang PT, Hardwick JP, Yun J, Janota D, Peng J, Kolz C, Guarini G, Wilson G, Shokolenko I, Stevens DA, Chilian WM.
PMID: 35039940
Basic Res Cardiol. 2022 Jan 17;117(1):3. doi: 10.1007/s00395-021-00908-1.

Endothelial dysfunction in diabetes is generally attributed to oxidative stress, but this view is challenged by observations showing antioxidants do not eliminate diabetic vasculopathy. As an alternative to oxidative stress-induced dysfunction, we interrogated if impaired mitochondrial function in endothelial...

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Kiyooka T, Ohanyan V, Yin L, et al. Mitochondrial DNA integrity and function are critical for endothelium-dependent vasodilation in rats with metabolic syndrome. Basic Res Cardiol. 2022;117(1):3doi: 10.1007/s00395-021-00908-1.
Kiyooka, T., Ohanyan, V., Yin, L., Pung, Y. F., Chen, Y. R., Chen, C. L., Kang, P. T., Hardwick, J. P., Yun, J., Janota, D., Peng, J., Kolz, C., Guarini, G., Wilson, G., Shokolenko, I., Stevens, D. A., & Chilian, W. M. (2022). Mitochondrial DNA integrity and function are critical for endothelium-dependent vasodilation in rats with metabolic syndrome. Basic research in cardiology, 117(1), 3. https://doi.org/10.1007/s00395-021-00908-1
Kiyooka, Takahiko, et al. "Mitochondrial DNA integrity and function are critical for endothelium-dependent vasodilation in rats with metabolic syndrome." Basic research in cardiology vol. 117,1 (2022): 3. doi: https://doi.org/10.1007/s00395-021-00908-1
Kiyooka T, Ohanyan V, Yin L, Pung YF, Chen YR, Chen CL, Kang PT, Hardwick JP, Yun J, Janota D, Peng J, Kolz C, Guarini G, Wilson G, Shokolenko I, Stevens DA, Chilian WM. Mitochondrial DNA integrity and function are critical for endothelium-dependent vasodilation in rats with metabolic syndrome. Basic Res Cardiol. 2022 Jan 17;117(1):3. doi: 10.1007/s00395-021-00908-1. PMID: 35039940.
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Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects.

Basic research in cardiology

Frenis K, Helmstädter J, Ruan Y, Schramm E, Kalinovic S, Kröller-Schön S, Bayo Jimenez MT, Hahad O, Oelze M, Jiang S, Wenzel P, Sommer CJ, Frauenknecht KBM, Waisman A, Gericke A, Daiber A, Münzel T, Steven S.
PMID: 33929610
Basic Res Cardiol. 2021 Apr 30;116(1):31. doi: 10.1007/s00395-021-00869-5.

Aircraft noise induces vascular and cerebral inflammation and oxidative stress causing hypertension and cardiovascular/cerebral dysfunction. With the present studies, we sought to determine the role of myeloid cells in the vascular vs. cerebral consequences of exposure to aircraft noise....

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Frenis K, Helmstädter J, Ruan Y, et al. Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects. Basic Res Cardiol. 2021;116(1):31doi: 10.1007/s00395-021-00869-5.
Frenis, K., Helmstädter, J., Ruan, Y., Schramm, E., Kalinovic, S., Kröller-Schön, S., Bayo Jimenez, M. T., Hahad, O., Oelze, M., Jiang, S., Wenzel, P., Sommer, C. J., Frauenknecht, K. B. M., Waisman, A., Gericke, A., Daiber, A., Münzel, T., & Steven, S. (2021). Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects. Basic research in cardiology, 116(1), 31. https://doi.org/10.1007/s00395-021-00869-5
Frenis, Katie, et al. "Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects." Basic research in cardiology vol. 116,1 (2021): 31. doi: https://doi.org/10.1007/s00395-021-00869-5
Frenis K, Helmstädter J, Ruan Y, Schramm E, Kalinovic S, Kröller-Schön S, Bayo Jimenez MT, Hahad O, Oelze M, Jiang S, Wenzel P, Sommer CJ, Frauenknecht KBM, Waisman A, Gericke A, Daiber A, Münzel T, Steven S. Ablation of lysozyme M-positive cells prevents aircraft noise-induced vascular damage without improving cerebral side effects. Basic Res Cardiol. 2021 Apr 30;116(1):31. doi: 10.1007/s00395-021-00869-5. PMID: 33929610; PMCID: PMC8087569.
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Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection.

Basic research in cardiology

Boulghobra D, Dubois M, Alpha-Bazin B, Coste F, Olmos M, Gayrard S, Bornard I, Meyer G, Gaillard JC, Armengaud J, Reboul C.
PMID: 34940922
Basic Res Cardiol. 2021 Dec 23;116(1):66. doi: 10.1007/s00395-021-00906-3.

Endothelial nitric oxide synthase (eNOS) activation in the heart plays a key role in exercise-induced cardioprotection during ischemia-reperfusion, but the underlying mechanisms remain unknown. We hypothesized that the cardioprotective effect of exercise training could be explained by the re-localization...

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Boulghobra D, Dubois M, Alpha-Bazin B, et al. Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection. Basic Res Cardiol. 2021;116(1):66doi: 10.1007/s00395-021-00906-3.
Boulghobra, D., Dubois, M., Alpha-Bazin, B., Coste, F., Olmos, M., Gayrard, S., Bornard, I., Meyer, G., Gaillard, J. C., Armengaud, J., & Reboul, C. (2021). Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection. Basic research in cardiology, 116(1), 66. https://doi.org/10.1007/s00395-021-00906-3
Boulghobra, Doria, et al. "Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection." Basic research in cardiology vol. 116,1 (2021): 66. doi: https://doi.org/10.1007/s00395-021-00906-3
Boulghobra D, Dubois M, Alpha-Bazin B, Coste F, Olmos M, Gayrard S, Bornard I, Meyer G, Gaillard JC, Armengaud J, Reboul C. Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection. Basic Res Cardiol. 2021 Dec 23;116(1):66. doi: 10.1007/s00395-021-00906-3. PMID: 34940922.
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Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation.

Basic research in cardiology

Chang Y, Li X, Cheng Q, Hu Y, Chen X, Hua X, Fan X, Tao M, Song J, Hu S.
PMID: 34870762
Basic Res Cardiol. 2021 Dec 06;116(1):64. doi: 10.1007/s00395-021-00904-5.

Acute rejection (AR) is an important contributor to graft failure, which remains a leading cause of death after heart transplantation (HTX). The regulation of immune metabolism has become a new hotspot in the development of immunosuppressive drugs. In this...

Cite
Chang Y, Li X, Cheng Q, et al. Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation. Basic Res Cardiol. 2021;116(1):64doi: 10.1007/s00395-021-00904-5.
Chang, Y., Li, X., Cheng, Q., Hu, Y., Chen, X., Hua, X., Fan, X., Tao, M., Song, J., & Hu, S. (2021). Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation. Basic research in cardiology, 116(1), 64. https://doi.org/10.1007/s00395-021-00904-5
Chang, Yuan, et al. "Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation." Basic research in cardiology vol. 116,1 (2021): 64. doi: https://doi.org/10.1007/s00395-021-00904-5
Chang Y, Li X, Cheng Q, Hu Y, Chen X, Hua X, Fan X, Tao M, Song J, Hu S. Single-cell transcriptomic identified HIF1A as a target for attenuating acute rejection after heart transplantation. Basic Res Cardiol. 2021 Dec 06;116(1):64. doi: 10.1007/s00395-021-00904-5. PMID: 34870762.
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A DARPin targeting activated Mac-1 is a novel diagnostic tool and potential anti-inflammatory agent in myocarditis, sepsis and myocardial infarction.

Basic research in cardiology

Siegel PM, Bojti I, Bassler N, Holien J, Flierl U, Wang X, Waggershauser P, Tonnar X, Vedecnik C, Lamprecht C, Stankova I, Li T, Helbing T, Wolf D, Anto-Michel N, Mitre LS, Ehrlich J, Orlean L, Bender I, Przewosnik A, Mauler M, Hollederer L, Moser M, Bode C, Parker MW, Peter K, Diehl P.
PMID: 33721106
Basic Res Cardiol. 2021 Mar 15;116(1):17. doi: 10.1007/s00395-021-00849-9.

The monocyte β

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Siegel PM, Bojti I, Bassler N, et al. A DARPin targeting activated Mac-1 is a novel diagnostic tool and potential anti-inflammatory agent in myocarditis, sepsis and myocardial infarction. Basic Res Cardiol. 2021;116(1):17doi: 10.1007/s00395-021-00849-9.
Siegel, P. M., Bojti, I., Bassler, N., Holien, J., Flierl, U., Wang, X., Waggershauser, P., Tonnar, X., Vedecnik, C., Lamprecht, C., Stankova, I., Li, T., Helbing, T., Wolf, D., Anto-Michel, N., Mitre, L. S., Ehrlich, J., Orlean, L., Bender, I., Przewosnik, A., Mauler, M., Hollederer, L., Moser, M., Bode, C., Parker, M. W., Peter, K., & Diehl, P. (2021). A DARPin targeting activated Mac-1 is a novel diagnostic tool and potential anti-inflammatory agent in myocarditis, sepsis and myocardial infarction. Basic research in cardiology, 116(1), 17. https://doi.org/10.1007/s00395-021-00849-9
Siegel, Patrick M, et al. "A DARPin targeting activated Mac-1 is a novel diagnostic tool and potential anti-inflammatory agent in myocarditis, sepsis and myocardial infarction." Basic research in cardiology vol. 116,1 (2021): 17. doi: https://doi.org/10.1007/s00395-021-00849-9
Siegel PM, Bojti I, Bassler N, Holien J, Flierl U, Wang X, Waggershauser P, Tonnar X, Vedecnik C, Lamprecht C, Stankova I, Li T, Helbing T, Wolf D, Anto-Michel N, Mitre LS, Ehrlich J, Orlean L, Bender I, Przewosnik A, Mauler M, Hollederer L, Moser M, Bode C, Parker MW, Peter K, Diehl P. A DARPin targeting activated Mac-1 is a novel diagnostic tool and potential anti-inflammatory agent in myocarditis, sepsis and myocardial infarction. Basic Res Cardiol. 2021 Mar 15;116(1):17. doi: 10.1007/s00395-021-00849-9. PMID: 33721106; PMCID: PMC7960600.
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