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TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway.

Experimental and therapeutic medicine

Meng L, Zhang Y, Li D, Shang X, Hao X, Chen X, Gao F.
PMID: 34335915
Exp Ther Med. 2021 Sep;22(3):973. doi: 10.3892/etm.2021.10405. Epub 2021 Jul 08.

Ischemic stroke seriously threatens human health and creates a large social burden. The present study investigated whether tissue inhibitor of metalloproteinases-3 (TIMP3) prevented cerebral ischemia/reperfusion (I/R), with the aim to explore the underlying mechanism. A transient middle cerebral artery...

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Meng L, Zhang Y, Li D, et al. TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway. Exp Ther Med. 2021;22(3):973doi: 10.3892/etm.2021.10405.
Meng, L., Zhang, Y., Li, D., Shang, X., Hao, X., Chen, X., & Gao, F. (2021). TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway. Experimental and therapeutic medicine, 22(3), 973. https://doi.org/10.3892/etm.2021.10405
Meng, Linglei, et al. "TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway." Experimental and therapeutic medicine vol. 22,3 (2021): 973. doi: https://doi.org/10.3892/etm.2021.10405
Meng L, Zhang Y, Li D, Shang X, Hao X, Chen X, Gao F. TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway. Exp Ther Med. 2021 Sep;22(3):973. doi: 10.3892/etm.2021.10405. Epub 2021 Jul 08. PMID: 34335915; PMCID: PMC8290470.
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Modulation of Cardiac Fibrosis in and Beyond Cells.

Frontiers in molecular biosciences

Fan D, Kassiri Z.
PMID: 34778374
Front Mol Biosci. 2021 Oct 27;8:750626. doi: 10.3389/fmolb.2021.750626. eCollection 2021.

The extracellular matrix (ECM) plays important roles in maintaining physiological structure and functions of various tissues and organs. Cardiac fibrosis is the excess deposition of ECM, including both fibrillar (collagens I and III) and non-fibrillar proteins. Characteristics of fibrosis...

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Fan D, Kassiri Z. Modulation of Cardiac Fibrosis in and Beyond Cells. Front Mol Biosci. 2021;8:750626doi: 10.3389/fmolb.2021.750626.
Fan, D., & Kassiri, Z. (2021). Modulation of Cardiac Fibrosis in and Beyond Cells. Frontiers in molecular biosciences, 8750626. https://doi.org/10.3389/fmolb.2021.750626
Fan, Dong, and Kassiri, Zamaneh. "Modulation of Cardiac Fibrosis in and Beyond Cells." Frontiers in molecular biosciences vol. 8 (2021): 750626. doi: https://doi.org/10.3389/fmolb.2021.750626
Fan D, Kassiri Z. Modulation of Cardiac Fibrosis in and Beyond Cells. Front Mol Biosci. 2021 Oct 27;8:750626. doi: 10.3389/fmolb.2021.750626. eCollection 2021. PMID: 34778374; PMCID: PMC8578679.
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CKAP4 participates in tryptase-induced phenotypic conversion in atrial fibroblasts through PAR2/p38/JNK pathway.

American journal of translational research

Tan H, Chen Z, Chen F, Xu W, Liu X.
PMID: 34017388
Am J Transl Res. 2021 Apr 15;13(4):2270-2282. eCollection 2021.

Our previous study found that tryptase activated atrial fibroblasts, increased collagen synthesis in atrial fibroblasts through protease activated receptor-2 (PAR2) receptors. Recent studies showed that cytoskeleton-associated protein 4 (CKAP4) played an important role in ventricular fibroblast activation. The present...

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Tan H, Chen Z, Chen F, et al. CKAP4 participates in tryptase-induced phenotypic conversion in atrial fibroblasts through PAR2/p38/JNK pathway. Am J Transl Res. 2021;13(4):2270-2282
Tan, H., Chen, Z., Chen, F., Xu, W., & Liu, X. (2021). CKAP4 participates in tryptase-induced phenotypic conversion in atrial fibroblasts through PAR2/p38/JNK pathway. American journal of translational research, 13(4), 2270-2282.
Tan, Hongwei, et al. "CKAP4 participates in tryptase-induced phenotypic conversion in atrial fibroblasts through PAR2/p38/JNK pathway." American journal of translational research vol. 13,4 (2021): 2270-2282.
Tan H, Chen Z, Chen F, Xu W, Liu X. CKAP4 participates in tryptase-induced phenotypic conversion in atrial fibroblasts through PAR2/p38/JNK pathway. Am J Transl Res. 2021 Apr 15;13(4):2270-2282. eCollection 2021. PMID: 34017388; PMCID: PMC8129387.
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Effects of coenzyme Q10 supplementation on inflammation, angiogenesis, and oxidative stress in breast cancer patients: a systematic review and meta-analysis of randomized controlled- trials.

Inflammopharmacology

Alimohammadi M, Rahimi A, Faramarzi F, Golpour M, Jafari-Shakib R, Alizadeh-Navaei R, Rafiei A.
PMID: 34008150
Inflammopharmacology. 2021 Jun;29(3):579-593. doi: 10.1007/s10787-021-00817-8. Epub 2021 May 18.

BACKGROUND/OBJECTIVE: Systemic inflammation and oxidative stress (OS) are associated with breast cancer. CoQ10 as an adjuvant treatment with conventional anti-cancer chemotherapy has been demonstrated to help in the inflammatory process and OS. This systematic review and meta-analysis of randomized...

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Alimohammadi M, Rahimi A, Faramarzi F, et al. Effects of coenzyme Q10 supplementation on inflammation, angiogenesis, and oxidative stress in breast cancer patients: a systematic review and meta-analysis of randomized controlled- trials. Inflammopharmacology. 2021;29(3):579-593doi: 10.1007/s10787-021-00817-8.
Alimohammadi, M., Rahimi, A., Faramarzi, F., Golpour, M., Jafari-Shakib, R., Alizadeh-Navaei, R., & Rafiei, A. (2021). Effects of coenzyme Q10 supplementation on inflammation, angiogenesis, and oxidative stress in breast cancer patients: a systematic review and meta-analysis of randomized controlled- trials. Inflammopharmacology, 29(3), 579-593. https://doi.org/10.1007/s10787-021-00817-8
Alimohammadi, Mina, et al. "Effects of coenzyme Q10 supplementation on inflammation, angiogenesis, and oxidative stress in breast cancer patients: a systematic review and meta-analysis of randomized controlled- trials." Inflammopharmacology vol. 29,3 (2021): 579-593. doi: https://doi.org/10.1007/s10787-021-00817-8
Alimohammadi M, Rahimi A, Faramarzi F, Golpour M, Jafari-Shakib R, Alizadeh-Navaei R, Rafiei A. Effects of coenzyme Q10 supplementation on inflammation, angiogenesis, and oxidative stress in breast cancer patients: a systematic review and meta-analysis of randomized controlled- trials. Inflammopharmacology. 2021 Jun;29(3):579-593. doi: 10.1007/s10787-021-00817-8. Epub 2021 May 18. PMID: 34008150.
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Relationships between Circulating Matrix Metalloproteinases, Tissue Inhibitor TIMP-2, and Renal Function in Patients with Myocarditis.

Kidney & blood pressure research

Kobusiak-Prokopowicz M, Kaaz K, Marciniak D, Karolko B, Mysiak A.
PMID: 34801997
Kidney Blood Press Res. 2021 Nov 19;1-9. doi: 10.1159/000519594. Epub 2021 Nov 19.

INTRODUCTION: Under physiological conditions, the myocardial extracellular matrix (ECM) is maintained by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). However, changes in the balance between MMPs and TIMPs can lead to pathological remodeling of the ECM, which...

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Kobusiak-Prokopowicz M, Kaaz K, Marciniak D, et al. Relationships between Circulating Matrix Metalloproteinases, Tissue Inhibitor TIMP-2, and Renal Function in Patients with Myocarditis. Kidney Blood Press Res. 2021;1-9doi: 10.1159/000519594.
Kobusiak-Prokopowicz, M., Kaaz, K., Marciniak, D., Karolko, B., & Mysiak, A. (2021). Relationships between Circulating Matrix Metalloproteinases, Tissue Inhibitor TIMP-2, and Renal Function in Patients with Myocarditis. Kidney & blood pressure research, 1-9. https://doi.org/10.1159/000519594
Kobusiak-Prokopowicz, Małgorzata, et al. "Relationships between Circulating Matrix Metalloproteinases, Tissue Inhibitor TIMP-2, and Renal Function in Patients with Myocarditis." Kidney & blood pressure research vol. (2021): 1-9. doi: https://doi.org/10.1159/000519594
Kobusiak-Prokopowicz M, Kaaz K, Marciniak D, Karolko B, Mysiak A. Relationships between Circulating Matrix Metalloproteinases, Tissue Inhibitor TIMP-2, and Renal Function in Patients with Myocarditis. Kidney Blood Press Res. 2021 Nov 19;1-9. doi: 10.1159/000519594. Epub 2021 Nov 19. PMID: 34801997.
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A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling.

Frontiers in cardiovascular medicine

Tan W, Li X, Zheng S, Li X, Zhang X, Pyle WG, Chen H, Wu J, Sun H, Zou Y, Backx PH, Yang FH.
PMID: 34150870
Front Cardiovasc Med. 2021 Jun 02;8:677727. doi: 10.3389/fcvm.2021.677727. eCollection 2021.

Heart failure is induced by multiple pathological mechanisms, and current therapies are ineffective against heart failure with preserved ejection fraction (HFpEF). As there are limited animal models of HFpEF, its underlying mechanisms have not yet been elucidated. Here, we...

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Tan W, Li X, Zheng S, et al. A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling. Front Cardiovasc Med. 2021;8:677727doi: 10.3389/fcvm.2021.677727.
Tan, W., Li, X., Zheng, S., Li, X., Zhang, X., Pyle, W. G., Chen, H., Wu, J., Sun, H., Zou, Y., Backx, P. H., & Yang, F. H. (2021). A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling. Frontiers in cardiovascular medicine, 8677727. https://doi.org/10.3389/fcvm.2021.677727
Tan, Weijiang, et al. "A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling." Frontiers in cardiovascular medicine vol. 8 (2021): 677727. doi: https://doi.org/10.3389/fcvm.2021.677727
Tan W, Li X, Zheng S, Li X, Zhang X, Pyle WG, Chen H, Wu J, Sun H, Zou Y, Backx PH, Yang FH. A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling. Front Cardiovasc Med. 2021 Jun 02;8:677727. doi: 10.3389/fcvm.2021.677727. eCollection 2021. PMID: 34150870; PMCID: PMC8206269.
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Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect.

Nutrition & metabolism

Zhou X, Yu L, Zhou M, Hou P, Yi L, Mi M.
PMID: 34147124
Nutr Metab (Lond). 2021 Jun 19;18(1):64. doi: 10.1186/s12986-021-00589-6.

BACKGROUND: This study investigated the mechanisms underlying the preventive effect of dihydromyricetin (DHM) against liver fibrosis involving hepatic stellate cells (HSCs) and hepatic natural killer (NK) cells.METHODS: A carbon tetrachloride (CClRESULTS: DHM ameliorated liver fibrosis in C57BL/6 mice, as...

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Zhou X, Yu L, Zhou M, et al. Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect. Nutr Metab (Lond). 2021;18(1):64doi: 10.1186/s12986-021-00589-6.
Zhou, X., Yu, L., Zhou, M., Hou, P., Yi, L., & Mi, M. (2021). Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect. Nutrition & metabolism, 18(1), 64. https://doi.org/10.1186/s12986-021-00589-6
Zhou, Xi, et al. "Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect." Nutrition & metabolism vol. 18,1 (2021): 64. doi: https://doi.org/10.1186/s12986-021-00589-6
Zhou X, Yu L, Zhou M, Hou P, Yi L, Mi M. Dihydromyricetin ameliorates liver fibrosis via inhibition of hepatic stellate cells by inducing autophagy and natural killer cell-mediated killing effect. Nutr Metab (Lond). 2021 Jun 19;18(1):64. doi: 10.1186/s12986-021-00589-6. PMID: 34147124; PMCID: PMC8214786.
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Resveratrol suppresses cholestasis-induced liver injury and fibrosis in rats associated with the inhibition of TGFβ1-Smad3-miR21 axis and profibrogenic and hepatic injury biomarkers.

Clinical and experimental pharmacology & physiology

ShamsEldeen AM, Al-Ani B, Ebrahim HA, Rashed L, Badr AM, Attia A, Farag AM, Kamar SS, Haidara MA, Al Humayed S, Ali Eshra M.
PMID: 34157155
Clin Exp Pharmacol Physiol. 2021 Oct;48(10):1402-1411. doi: 10.1111/1440-1681.13546. Epub 2021 Jul 13.

Cholestasis caused by slowing or blockage of bile flow is a serious liver disease that can lead to liver fibrosis and cirrhosis. The link between transforming growth factor beta 1 (TGFβ1), Smad family member 3 (Smad3), and microRNA 21...

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ShamsEldeen AM, Al-Ani B, Ebrahim HA, et al. Resveratrol suppresses cholestasis-induced liver injury and fibrosis in rats associated with the inhibition of TGFβ1-Smad3-miR21 axis and profibrogenic and hepatic injury biomarkers. Clin Exp Pharmacol Physiol. 2021;48(10):1402-1411doi: 10.1111/1440-1681.13546.
ShamsEldeen, A. M., Al-Ani, B., Ebrahim, H. A., Rashed, L., Badr, A. M., Attia, A., Farag, A. M., Kamar, S. S., Haidara, M. A., Al Humayed, S., & Ali Eshra, M. (2021). Resveratrol suppresses cholestasis-induced liver injury and fibrosis in rats associated with the inhibition of TGFβ1-Smad3-miR21 axis and profibrogenic and hepatic injury biomarkers. Clinical and experimental pharmacology & physiology, 48(10), 1402-1411. https://doi.org/10.1111/1440-1681.13546
ShamsEldeen, Asmaa M, et al. "Resveratrol suppresses cholestasis-induced liver injury and fibrosis in rats associated with the inhibition of TGFβ1-Smad3-miR21 axis and profibrogenic and hepatic injury biomarkers." Clinical and experimental pharmacology & physiology vol. 48,10 (2021): 1402-1411. doi: https://doi.org/10.1111/1440-1681.13546
ShamsEldeen AM, Al-Ani B, Ebrahim HA, Rashed L, Badr AM, Attia A, Farag AM, Kamar SS, Haidara MA, Al Humayed S, Ali Eshra M. Resveratrol suppresses cholestasis-induced liver injury and fibrosis in rats associated with the inhibition of TGFβ1-Smad3-miR21 axis and profibrogenic and hepatic injury biomarkers. Clin Exp Pharmacol Physiol. 2021 Oct;48(10):1402-1411. doi: 10.1111/1440-1681.13546. Epub 2021 Jul 13. PMID: 34157155.
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EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis.

The Journal of cell biology

Nanba D, Toki F, Asakawa K, Matsumura H, Shiraishi K, Sayama K, Matsuzaki K, Toki H, Nishimura EK.
PMID: 34550317
J Cell Biol. 2021 Nov 01;220(11). doi: 10.1083/jcb.202012073. Epub 2021 Sep 22.

Skin regenerative capacity declines with age, but the underlying mechanisms are largely unknown. Here we demonstrate a functional link between epidermal growth factor receptor (EGFR) signaling and type XVII collagen (COL17A1) proteolysis on age-associated alteration of keratinocyte stem cell...

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Nanba D, Toki F, Asakawa K, et al. EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis. J Cell Biol. 2021;220(11)doi: 10.1083/jcb.202012073.
Nanba, D., Toki, F., Asakawa, K., Matsumura, H., Shiraishi, K., Sayama, K., Matsuzaki, K., Toki, H., & Nishimura, E. K. (2021). EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis. The Journal of cell biology, 220(11), . https://doi.org/10.1083/jcb.202012073
Nanba, Daisuke, et al. "EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis." The Journal of cell biology vol. 220,11 (2021). doi: https://doi.org/10.1083/jcb.202012073
Nanba D, Toki F, Asakawa K, Matsumura H, Shiraishi K, Sayama K, Matsuzaki K, Toki H, Nishimura EK. EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis. J Cell Biol. 2021 Nov 01;220(11). doi: 10.1083/jcb.202012073. Epub 2021 Sep 22. PMID: 34550317; PMCID: PMC8563287.
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Atypical response to bacterial coinfection and persistent neutrophilic bronchoalveolar inflammation distinguish critical COVID-19 from influenza.

JCI insight

Cambier S, Metzemaekers M, de Carvalho AC, Nooyens A, Jacobs C, Vanderbeke L, Malengier-Devlies B, Gouwy M, Heylen E, Meersseman P, Hermans G, Wauters E, Wilmer A, Schols D, Matthys P, Opdenakker G, Marques RE, Wauters J, Vandooren J, Proost P.
PMID: 34793331
JCI Insight. 2022 Jan 11;7(1). doi: 10.1172/jci.insight.155055.

Neutrophils are recognized as important circulating effector cells in the pathophysiology of severe coronavirus disease 2019 (COVID-19). However, their role within the inflamed lungs is incompletely understood. Here, we collected bronchoalveolar lavage (BAL) fluids and parallel blood samples of...

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Cambier S, Metzemaekers M, de Carvalho AC, et al. Atypical response to bacterial coinfection and persistent neutrophilic bronchoalveolar inflammation distinguish critical COVID-19 from influenza. JCI Insight. 2022;7(1)doi: 10.1172/jci.insight.155055.
Cambier, S., Metzemaekers, M., de Carvalho, A. C., Nooyens, A., Jacobs, C., Vanderbeke, L., Malengier-Devlies, B., Gouwy, M., Heylen, E., Meersseman, P., Hermans, G., Wauters, E., Wilmer, A., Schols, D., Matthys, P., Opdenakker, G., Marques, R. E., Wauters, J., Vandooren, J., & Proost, P. (2022). Atypical response to bacterial coinfection and persistent neutrophilic bronchoalveolar inflammation distinguish critical COVID-19 from influenza. JCI insight, 7(1), . https://doi.org/10.1172/jci.insight.155055
Cambier, Seppe, et al. "Atypical response to bacterial coinfection and persistent neutrophilic bronchoalveolar inflammation distinguish critical COVID-19 from influenza." JCI insight vol. 7,1 (2022). doi: https://doi.org/10.1172/jci.insight.155055
Cambier S, Metzemaekers M, de Carvalho AC, Nooyens A, Jacobs C, Vanderbeke L, Malengier-Devlies B, Gouwy M, Heylen E, Meersseman P, Hermans G, Wauters E, Wilmer A, Schols D, Matthys P, Opdenakker G, Marques RE, Wauters J, Vandooren J, Proost P. Atypical response to bacterial coinfection and persistent neutrophilic bronchoalveolar inflammation distinguish critical COVID-19 from influenza. JCI Insight. 2022 Jan 11;7(1). doi: 10.1172/jci.insight.155055. PMID: 34793331.
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