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Matrix Components, supplied by Genovis Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses <t>extracellular</t> signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.
Extracellular Matrix Component, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses <t>extracellular</t> signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses <t>extracellular</t> signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses <t>extracellular</t> signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses <t>extracellular</t> signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.
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matrix components  (Angiocrine)
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses <t>extracellular</t> signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.
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Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses extracellular signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.

Journal: Nutrients

Article Title: Therapeutic Modulation of Mitophagy by Cafestol in Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis

doi: 10.3390/nu17233680

Figure Lengend Snippet: Schematic overview of cafestol’s mechanistic actions. This schematic illustrates the integrated molecular pathways through which cafestol safeguards cardiac function. Cafestol activates the liver kinase B1 (LKB1)–AMP-activated protein kinase (AMPK) –Unc-51 like autophagy activating kinase 1 (ULK1; mammalian homolog of autophagy-related protein 1 [Atg1]) axis and promotes PTEN-induced kinase 1 (PINK1)–Parkin–sequestosome 1 (p62)–mediated mitophagy, facilitating mitochondrial turnover and alleviating organelle stress. In parallel, cafestol enhances nuclear factor erythroid 2–related factor 2 (Nrf2)–driven antioxidant defenses. Upon oxidative stress, Nrf2 translocates into the nucleus and binds to the antioxidant response element (ARE), initiating transcription of antioxidant and cytoprotective genes including heme oxygenase-1 (HO-1), superoxide gismutase (SOD), catalase (CAT), glutathione peroxidase 1 (GPx1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutathione S-transferase (GST), and Maf1 homolog (m1). Concurrently, cafestol suppresses extracellular signal-regulated kinase (ERK) and mammalian target of rapamycin (mTOR) signaling associated with fibrosis and endoplasmic reticulum stress. Collectively, these actions preserve mitochondrial integrity, limit collagen deposition, and attenuate cardiac hypertrophy and fibrosis. Ub denotes ubiquitin. Blue arrows denote activation; red hammer lines indicate inhibition; black arrows represent stimulation; and double arrows signify restoration of impaired signaling.

Article Snippet: Additional targets included collagen I (Santa Cruz Biotechnology, Dallas, TX, USA; Cat# sc-59772), a key extracellular matrix component; GAPDH (Cell Signaling Technology, Danvers, MA, USA; Cat# 2118), used as a loading control; and apoptosis-related proteins Bcl-2, Bax, and cleaved caspase-3.

Techniques: Ubiquitin Proteomics, Activation Assay, Inhibition