new figures from pmc; updated config and log

figure_fetch.log

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 2024-10-03 03:25:44 - ==========================================================
 
+2024-10-03 04:22:04 - Starting NCBI PMC Figure Fetcher
+
+2024-10-03 04:22:04 - Configuration loaded from query_config.yml
+
+2024-10-03 04:22:04 - Final stretch, then deactivating cycle.
+
+2024-10-03 04:22:05 - PMC search query: (((((((((((signaling pathway[Figure/Table Caption]) OR signalling pathway[Figure/Table Caption]) OR regulatory pathway[Figure/Table Caption]) OR disease pathway[Figure/Table Caption]) OR drug pathway[Figure/Table Caption]) OR metabolic pathway[Figure/Table Caption]) OR biosynthetic pathway[Figure/Table Caption]) OR synthesis pathway[Figure/Table Caption]) OR cancer pathway[Figure/Table Caption]) OR response pathway[Figure/Table Caption]) OR cycle pathway[Figure/Table Caption])) AND (2024/09/01[PUBDATE] : 3000/01/01[PUBDATE])
+
+2024-10-03 04:22:17 - PMC search completed. Fetched 668 results (max set to 3000).
+
+2024-10-03 04:22:21 - Extracted 531 figures from XML content.
+
+2024-10-03 04:22:21 - Identified 174 pathway figures.
+
+2024-10-03 04:22:21 - Skipped 6 figures previously processed.
+
+2024-10-03 04:22:21 - Processed 168 pathway figures for download.
+
+2024-10-03 04:24:38 - New pathway figures downloaded: 168
+
+2024-10-03 04:24:38 - NCBI PMC Figure Fetcher completed
+
+2024-10-03 04:24:38 - ==========================================================
+

figures/PMC11385095__jciinsight-9-177729-g215.yml

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+---
+figid: PMC11385095__jciinsight-9-177729-g215
+pmcid: PMC11385095
+image_filename: jciinsight-9-177729-g215.jpg
+figure_link: /pmc/articles/PMC11385095/figure/F5/
+number: Figure 5
+figure_title: Comparison of NP- and tonsil-derived ASCs
+caption: (A) Violin plots of genes upregulated in NP- and tonsil-derived ASCs. (B)
+  GO biological process performed on most variable genes in ASCs derived from NPs
+  and tonsils. Wilcoxon’s test was used for gene comparisons. (C) GSEA was performed
+  on the top 2,000 most variable features in ASCs derived from NPs and tonsils. NF-κB
+  ranked as the most-enriched signaling pathway in NPs
+article_title: Increased autoreactivity and maturity of EBI2+ antibody-secreting cells
+  from nasal polyps
+citation: Junqin Bai, et al. JCI Insight. 2024 Sep 10;9(17).
+year: '2024'
+pub_date: 2024-9-10
+epub_date: 2024-9-10
+doi: 10.1172/jci.insight.177729
+journal_title: JCI Insight
+journal_nlm_ta: JCI Insight
+publisher_name: American Society for Clinical Investigation
+keywords:
+- Immunology
+- Inflammation
+- Adaptive immunity
+- Immunoglobulins
+- Respiration
+---

figures/PMC11387088__CRP2024-1905996.004.yml

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+---
+figid: PMC11387088__CRP2024-1905996.004
+pmcid: PMC11387088
+image_filename: CRP2024-1905996.004.jpg
+figure_link: /pmc/articles/PMC11387088/figure/F4/
+number: Figure 4
+figure_title: Inhibiting H2AX can suppress the expression of p-JNK and mitochondrial
+  autophagy and fusion, as well as attenuate apoptosis in cardiac myocytes through
+  the P53/SHP2 signaling pathway.
+caption: Inhibiting H2AX can suppress the expression of p-JNK and mitochondrial autophagy
+  and fusion, as well as attenuate apoptosis in cardiac myocytes through the P53/SHP2
+  signaling pathway. (a) Western blotting and relative expression of p-H2AX, P53,
+  p-JNK, SHP, p-SHP2, and p-RAS. (b) Western blotting and relative expression of parkin,
+  Drp1, Cyt-C, Caspase-3, and Caspase-8. ∗∗P < 0.001. (c) Western blot grayscale statistics
+article_title: Inhibiting H2AX Can Ameliorate Myocardial Ischemia/Reperfusion Injury
+  by Regulating P53/JNK Signaling Pathway
+citation: Ziyang Yu, et al. Cardiol Res Pract. 2024;2024(NA).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-9-3
+doi: 10.1155/2024/1905996
+journal_title: Cardiology Research and Practice
+journal_nlm_ta: Cardiol Res Pract
+publisher_name: Wiley
+keywords: []
+---

figures/PMC11387088__CRP2024-1905996.005.yml

@@ -0,0 +1,22 @@
+---
+figid: PMC11387088__CRP2024-1905996.005
+pmcid: PMC11387088
+image_filename: CRP2024-1905996.005.jpg
+figure_link: /pmc/articles/PMC11387088/figure/F5/
+number: Figure 5
+figure_title: Inhibiting H2AX Can Ameliorate Myocardial Ischemia/Reperfusion Injury
+  by Regulating P53/JNK Signaling Pathway
+caption: H2AX mediates myocardial ischemia/reperfusion injury by regulating P53 and
+  JNK signaling pathways
+article_title: Inhibiting H2AX Can Ameliorate Myocardial Ischemia/Reperfusion Injury
+  by Regulating P53/JNK Signaling Pathway
+citation: Ziyang Yu, et al. Cardiol Res Pract. 2024;2024(NA).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-9-3
+doi: 10.1155/2024/1905996
+journal_title: Cardiology Research and Practice
+journal_nlm_ta: Cardiol Res Pract
+publisher_name: Wiley
+keywords: []
+---

figures/PMC11387119__ijo-65-04-05687-g02.yml

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+---
+figid: PMC11387119__ijo-65-04-05687-g02
+pmcid: PMC11387119
+image_filename: ijo-65-04-05687-g02.jpg
+figure_link: /pmc/articles/PMC11387119/figure/F3/
+number: Figure 3
+figure_title: Inflammasome sensors have diverse roles in tumorigenesis.
+caption: Inflammasome sensors have diverse roles in tumorigenesis. The NLRP1b, NLRP3
+  and NLRP6 inflammasomes facilitate the production of IL-18, which helps protect
+  against colorectal cancer associated with colitis. IL-18 also triggers the anticancer
+  activity of natural killer cells against metastatic colonic tumor cells, reduces
+  the levels of IL-22BP and may prevent the establishment of colitis-inducing microbiota,
+  potentially through its impact on MUC2 secretion by goblet cells. The NLRP3 inflammasome,
+  along with the IL-1β/IL-1 receptor signaling pathway, drives a T-cell response against
+  transplantable tumor cells. In mice, NAIP1-6 proteins regulate STAT3 phosphorylation
+  and the transcription of genes involved in anti-apoptotic and cell proliferation
+  mechanisms. NLRC4 inhibits melanoma growth by enhancing macrophage inflammation
+  and increasing IFNγ production in T cells. AIM2 suppresses AKT and cMyc phosphorylation,
+  limiting stem cell proliferation and preventing colonization by colitis-promoting
+  microbiota (83). AIM2, absent in melanoma 2; IL-22BP, IL-22 binding protein; MUC2,
+  mucin 2; NLRC4, Nod-like receptor C4; NOD, nucleotide-binding oligomerization domain;
+  NLRP, NLR family pyrin domain containing
+article_title: NLRC4, inflammation and colorectal cancer (Review)
+citation: Guojun Tong, et al. Int J Oncol. 2024 Oct;65(4).
+year: '2024'
+pub_date: 2024-10-
+epub_date: 2024-9-04
+doi: 10.3892/ijo.2024.5687
+journal_title: International Journal of Oncology
+journal_nlm_ta: Int J Oncol
+publisher_name: D.A. Spandidos
+keywords:
+- Nod-like receptor C4
+- colorectal cancer
+- prognosis
+- mechanism of action
+- signaling pathway
+---

figures/PMC11387478__41420_2024_2169_Figa_HTML.yml

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+---
+figid: PMC11387478__41420_2024_2169_Figa_HTML
+pmcid: PMC11387478
+image_filename: 41420_2024_2169_Figa_HTML.jpg
+figure_link: /pmc/articles/PMC11387478/figure/FNA/
+number: .na.character
+figure_title: HIRI is a thorny problem after liver surgery such as liver transplantation.
+caption: HIRI is a thorny problem after liver surgery such as liver transplantation.
+  In a murine model of HIRI, MSC-EVs enriched GAS6 effectively enhance macrophage
+  efferocytosis both in vivo and in vitro through the GAS6/MerTK/ERK/COX2 signaling
+  pathway and significantly mitigate liver injury. This image was drawn by the authors
+article_title: Extracellular vesicles containing GAS6 protect the liver from ischemia-reperfusion
+  injury by enhancing macrophage efferocytosis via MerTK-ERK-COX2 signaling
+citation: Longyu Miao, et al. Cell Death Discov. 2024;10(NA).
+year: '2024'
+pub_date: 2024--
+epub_date: 2024-9-10
+doi: 10.1038/s41420-024-02169-y
+journal_title: Cell Death Discovery
+journal_nlm_ta: Cell Death Discov
+publisher_name: Nature Publishing Group UK
+keywords:
+- Mesenchymal stem cells
+- Protein-protein interaction networks
+- Liver fibrosis
+---

figures/PMC11391519__mmr-30-05-13321-g01.yml

@@ -0,0 +1,29 @@
+---
+figid: PMC11391519__mmr-30-05-13321-g01
+pmcid: PMC11391519
+image_filename: mmr-30-05-13321-g01.jpg
+figure_link: /pmc/articles/PMC11391519/figure/F2/
+number: Figure 2.
+figure_title: I/R injury inhibited the expression of the PI3K/AKT signaling pathway.
+caption: I/R injury inhibited the expression of the PI3K/AKT signaling pathway. (A)
+  The protein expression of PI3K and AKT and the activity of phosphorylated AKT in
+  rat myocardium was detected by western blotting. (B) The protein expression of PI3K
+  and AKT and the activity of phosphorylated AKT in H9C2 cells was detected by western
+  blotting. *P<0.05, **P<0.01, n=3. PI3K, phosphatidylinositol-3-hydroxykinase; AKT,
+  serine/threonine kinase; NC, negative control; H/R, hypoxia and reoxygenation
+article_title: Effects of STAT4 on myocardial ischemia‑reperfusion injury and the
+  underlying mechanisms
+citation: Mei He, et al. Mol Med Rep. 2024 Nov;30(5).
+year: '2024'
+pub_date: 2024-11-
+epub_date: 2024-9-02
+doi: 10.3892/mmr.2024.13321
+journal_title: Molecular Medicine Reports
+journal_nlm_ta: Mol Med Rep
+publisher_name: D.A. Spandidos
+keywords:
+- signal transducer and activator of transcription 4
+- myocardium
+- ischemia-reperfusion
+- apoptosis
+---

figures/PMC11391519__mmr-30-05-13321-g04.yml

@@ -0,0 +1,28 @@
+---
+figid: PMC11391519__mmr-30-05-13321-g04
+pmcid: PMC11391519
+image_filename: mmr-30-05-13321-g04.jpg
+figure_link: /pmc/articles/PMC11391519/figure/F5/
+number: Figure 5.
+figure_title: Overexpression of STAT4 can activate the PI3K/AKT signaling pathway
+  in H9C2 cells.
+caption: Overexpression of STAT4 can activate the PI3K/AKT signaling pathway in H9C2
+  cells. Western blotting results for PI3K and AKT after lentivirus infection and
+  H/R treatment. *P<0.05, n=3. PI3K, phosphatidylinositol-3-hydroxykinase; AKT, serine/threonine
+  kinase; H/R, hypoxia and reoxygenation; NC, negative control
+article_title: Effects of STAT4 on myocardial ischemia‑reperfusion injury and the
+  underlying mechanisms
+citation: Mei He, et al. Mol Med Rep. 2024 Nov;30(5).
+year: '2024'
+pub_date: 2024-11-
+epub_date: 2024-9-02
+doi: 10.3892/mmr.2024.13321
+journal_title: Molecular Medicine Reports
+journal_nlm_ta: Mol Med Rep
+publisher_name: D.A. Spandidos
+keywords:
+- signal transducer and activator of transcription 4
+- myocardium
+- ischemia-reperfusion
+- apoptosis
+---

figures/PMC11393989__cells-13-01493-g001.yml

@@ -0,0 +1,38 @@
+---
+figid: PMC11393989__cells-13-01493-g001
+pmcid: PMC11393989
+image_filename: cells-13-01493-g001.jpg
+figure_link: /pmc/articles/PMC11393989/figure/F1/
+number: Figure 1
+figure_title: Molecular and cellular mechanisms of TGF-β signaling pathway in GO.
+caption: Molecular and cellular mechanisms of TGF-β signaling pathway in GO. TGF-β
+  exerts its multifaceted effects on fibrosis and inflammation through both canonical
+  and non-canonical signaling pathways. It binds to TGFR2, subsequently activating
+  TGFR1. In the canonical pathway, TGFR1 phosphorylates Smad2 and Smad3, enabling
+  their complex formation with Smad4. This complex then translocates to the nucleus,
+  initiating transcription of fibrogenic genes. In non-canonical signaling pathways,
+  TGF-β promotes fibrosis and ECM deposition by activating mitogen-activated protein
+  kinase (MAPK) pathways, phosphoinositide 3-kinase (PI3K) pathways, RhoA-GTPase pathways,
+  Wnt/β-catenin pathways, and NOX4 pathways. In the MAPK pathways, phosphorylated
+  p38/JNK also interacts with the canonical pathway by activating Smad2 and Smad3,
+  c-Jun, and AP-1. Additionally, in the Wnt/β-catenin pathway, Wnt ligands bind to
+  the FZD and LRP5/6 receptors, leading to increased levels of β-catenin. β-catenin
+  then translocates to the nucleus to induce target gene expression. The blue arrow
+  indicates an activating effect, while the red T-bar signifies an inhibitory effect
+article_title: A Review of Pathophysiology and Therapeutic Strategies Targeting TGF-β
+  in Graves’ Ophthalmopathy
+citation: Hsin-Ho Chang, et al. Cells. 2024 Sep;13(17).
+year: '2024'
+pub_date: 2024-9-
+epub_date: 2024-9-05
+doi: 10.3390/cells13171493
+journal_title: Cells
+journal_nlm_ta: Cells
+publisher_name: MDPI
+keywords:
+- Graves’ ophthalmopathy (GO)
+- transforming growth factor-β (TGF-β)
+- orbital fibrosis
+- extracellular matrix (ECM)
+- orbital fibroblast
+---

figures/PMC11394487__cells-13-01474-g001.yml

@@ -0,0 +1,38 @@
+---
+figid: PMC11394487__cells-13-01474-g001
+pmcid: PMC11394487
+image_filename: cells-13-01474-g001.jpg
+figure_link: /pmc/articles/PMC11394487/figure/F1/
+number: Figure 1
+figure_title: The tumor microenvironment pathway is predicted to be altered (z-score
+  = −2.
+caption: 'The tumor microenvironment pathway is predicted to be altered (z-score =
+  −2.77) and closely associated [−log(p-value) = 8.83] with breast cancer. Description:
+  AKT activates NFκB and SLC2 and inhibits BAD and FOXO via phosphorylation, where
+  BAD and FOXO induce the apoptosis of tumor cells. ARG1 contributes to CD8 T-cell
+  immunity; BCL2 promotes the survival of tumor cells; CCL2, CSF1, CSF2, and CSF3
+  enhance myeloid-derived suppressor cell accumulation and the proliferation of tumor-associated
+  macrophages; CCND1 stimulates the proliferation of tumor cells; CD274 is responsible
+  for the adaptive immune response of CD8+ T cells; CTL promotes apoptosis; and PD-1
+  is involved in the PD-L1 cancer immunotherapy pathway. CXCL12, CFCL8, FGF, MMP9,
+  OSM, and VEGF are causative for angiogenesis. STAT3 regulates the expression of
+  BCL2, CCND1, CD274, FAS, HIF1A, MMP2, MYC, PTGS2, SPP1, and VEGF, whereas NFκB regulates
+  the expression of AP1, BCL2, CD274, CFLAR, and PLAU, which are responsible for tumor
+  cell proliferation, viability, angiogenesis, and metastasis'
+article_title: Unraveling the Mystery of Energy-Sensing Enzymes and Signaling Pathways
+  in Tumorigenesis and Their Potential as Therapeutic Targets for Cancer
+citation: Zeenat Mirza, et al. Cells. 2024 Sep;13(17).
+year: '2024'
+pub_date: 2024-9-
+epub_date: 2024-9-02
+doi: 10.3390/cells13171474
+journal_title: Cells
+journal_nlm_ta: Cells
+publisher_name: MDPI
+keywords:
+- cancer
+- energy-sensing enzymes
+- genes and signaling pathways
+- Warburg effect
+- anticancer drug
+---

figures/PMC11394487__cells-13-01474-g002.yml

@@ -0,0 +1,27 @@
+---
+figid: PMC11394487__cells-13-01474-g002
+pmcid: PMC11394487
+image_filename: cells-13-01474-g002.jpg
+figure_link: /pmc/articles/PMC11394487/figure/F2/
+number: Figure 2
+figure_title: Mitochondrial biogenesis pathways.
+caption: Mitochondrial biogenesis pathways. Downregulation of differentially expressed
+  genes ACSS2, CHD9, IDH2, SOD2, MEF2C, PPARA, PPARGC1A, and PPARGC1B causes inhibition
+  of the mitochondrial biogenesis process in breast cancer
+article_title: Unraveling the Mystery of Energy-Sensing Enzymes and Signaling Pathways
+  in Tumorigenesis and Their Potential as Therapeutic Targets for Cancer
+citation: Zeenat Mirza, et al. Cells. 2024 Sep;13(17).
+year: '2024'
+pub_date: 2024-9-
+epub_date: 2024-9-02
+doi: 10.3390/cells13171474
+journal_title: Cells
+journal_nlm_ta: Cells
+publisher_name: MDPI
+keywords:
+- cancer
+- energy-sensing enzymes
+- genes and signaling pathways
+- Warburg effect
+- anticancer drug
+---

figures/PMC11394487__cells-13-01474-g003.yml

@@ -0,0 +1,30 @@
+---
+figid: PMC11394487__cells-13-01474-g003
+pmcid: PMC11394487
+image_filename: cells-13-01474-g003.jpg
+figure_link: /pmc/articles/PMC11394487/figure/F3/
+number: Figure 3
+figure_title: Unraveling the Mystery of Energy-Sensing Enzymes and Signaling Pathways
+  in Tumorigenesis and Their Potential as Therapeutic Targets for Cancer
+caption: Integration of energy metabolism includes multiple events and pathways such
+  as glucagon signaling in metabolic pathways, PKA-mediated phosphorylation, insulin
+  stimulating increased expression of xylulose-5-phosphate (Xy-5-P), the AMP kinase
+  (AMPK)-mediated response to elevated AMP, dephosphorylation of key metabolic factors
+  by PP2A, and the transcriptional activation of metabolic genes by ChREBP
+article_title: Unraveling the Mystery of Energy-Sensing Enzymes and Signaling Pathways
+  in Tumorigenesis and Their Potential as Therapeutic Targets for Cancer
+citation: Zeenat Mirza, et al. Cells. 2024 Sep;13(17).
+year: '2024'
+pub_date: 2024-9-
+epub_date: 2024-9-02
+doi: 10.3390/cells13171474
+journal_title: Cells
+journal_nlm_ta: Cells
+publisher_name: MDPI
+keywords:
+- cancer
+- energy-sensing enzymes
+- genes and signaling pathways
+- Warburg effect
+- anticancer drug
+---