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(A,B) Compared to the high-fat diet (HFD) group, supplementation with <t>CTRP3</t> significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).
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(A,B) Compared to the high-fat diet (HFD) group, supplementation with <t>CTRP3</t> significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).
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(A,B) Compared to the high-fat diet (HFD) group, supplementation with <t>CTRP3</t> significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).
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(A,B) Compared to the high-fat diet (HFD) group, supplementation with <t>CTRP3</t> significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).
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(A,B) Compared to the high-fat diet (HFD) group, supplementation with <t>CTRP3</t> significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).
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(A) Representative whole-femur μCT isosurface renderings at 5, 10 and 20dpf for <t>CTRP3</t> KO, WT and TG mice. Femurs were scanned after removal of intramedullary pins. Apparent bends in 5dpf bones are artifacts of this removal: fractures are straight in vivo. Quantitative callus μCT data for (B) bone volume fraction (BV/TV), (C) bone mineral content (BMC) and (D) bone mineral density (BMD). Solid lines represent p<0.05 by genotype. Maroon up-arrows represent female mice and navy down-arrows represent male mice. For additional quantitative measures of calluses, see Fig S1.
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(A) Representative whole-femur μCT isosurface renderings at 5, 10 and 20dpf for <t>CTRP3</t> KO, WT and TG mice. Femurs were scanned after removal of intramedullary pins. Apparent bends in 5dpf bones are artifacts of this removal: fractures are straight in vivo. Quantitative callus μCT data for (B) bone volume fraction (BV/TV), (C) bone mineral content (BMC) and (D) bone mineral density (BMD). Solid lines represent p<0.05 by genotype. Maroon up-arrows represent female mice and navy down-arrows represent male mice. For additional quantitative measures of calluses, see Fig S1.
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Image Search Results


(A,B) Compared to the high-fat diet (HFD) group, supplementation with CTRP3 significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A,B) Compared to the high-fat diet (HFD) group, supplementation with CTRP3 significantly improves cardiac function in mice, as evidenced by enhanced left ventricular ejection fraction. (C,D) Histological examination of myocardial tissue reveals substantial lipid droplet accumulation in the HFD group. However, CTRP3 supplementation reduces lipid droplet accumulation, improves myocardial tissue structure, and alleviates the degree of fibrosis. (E–M) Immunofluorescence results indicate that CTRP3 supplementation mitigates myocardial inflammation, apoptosis, and oxidative stress in mice. (N–Q) Serum ELISA assays demonstrate that levels of triglycerides (TG), total cholesterol (TCHO), inflammatory markers, apoptotic factors, and oxidative stress indicators are significantly improved in the CTRP3 group compared to the HFD group ( n ≥ 3, p < 0.05).

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: Immunofluorescence, Enzyme-linked Immunosorbent Assay

(A–F) Lipid testing results demonstrate that palmitic acid (PA) induces lipid accumulation in myocardial cells, while CTRP3 supplementation significantly reduces lipid droplet accumulation. (G) CTRP3 intervention improves the expression of genes related to fatty acid uptake, fatty acid oxidation, and lipid efflux in myocardial cells ( n ≥ 3, p < 0.05). (H) Quantitative PCR (q-PCR) results indicate that CTRP3 mitigates inflammation, apoptosis, and oxidative stress in myocardial cells stimulated by PA ( n ≥ 3, p < 0.05).

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A–F) Lipid testing results demonstrate that palmitic acid (PA) induces lipid accumulation in myocardial cells, while CTRP3 supplementation significantly reduces lipid droplet accumulation. (G) CTRP3 intervention improves the expression of genes related to fatty acid uptake, fatty acid oxidation, and lipid efflux in myocardial cells ( n ≥ 3, p < 0.05). (H) Quantitative PCR (q-PCR) results indicate that CTRP3 mitigates inflammation, apoptosis, and oxidative stress in myocardial cells stimulated by PA ( n ≥ 3, p < 0.05).

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: Expressing, Real-time Polymerase Chain Reaction

(A–E) RNA sequencing analysis of myocardial tissue from the control group, HFD group, and CTRP3 group indicates that CTRP3 likely exerts its effects within myocardial mitochondria, playing a role in the metabolic regulation of myocardial lipotoxicity.

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A–E) RNA sequencing analysis of myocardial tissue from the control group, HFD group, and CTRP3 group indicates that CTRP3 likely exerts its effects within myocardial mitochondria, playing a role in the metabolic regulation of myocardial lipotoxicity.

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: RNA Sequencing, Control

(A,B) JC-1 staining results demonstrate a decrease in mitochondrial membrane potential in myocardial cells of the PA group. (C,D) Mito-Tracker staining results show a reduction in mitochondrial number in the PA group. (E) PA intervention in myocardial cells leads to decreased ATP production, while CTRP3 intervention improves ATP generation. (F) Transmission electron microscopy reveals increased mitochondrial damage and autophagy in myocardial cells following PA intervention. CTRP3 can mitigate mitochondrial damage and autophagy in myocardial cells.

Journal: Frontiers in Cardiovascular Medicine

Article Title: CTRP3 attenuates myocardial lipotoxicity via suppression of lipid accumulation, inflammation, apoptosis, and mitochondrial oxidative stress

doi: 10.3389/fcvm.2025.1575929

Figure Lengend Snippet: (A,B) JC-1 staining results demonstrate a decrease in mitochondrial membrane potential in myocardial cells of the PA group. (C,D) Mito-Tracker staining results show a reduction in mitochondrial number in the PA group. (E) PA intervention in myocardial cells leads to decreased ATP production, while CTRP3 intervention improves ATP generation. (F) Transmission electron microscopy reveals increased mitochondrial damage and autophagy in myocardial cells following PA intervention. CTRP3 can mitigate mitochondrial damage and autophagy in myocardial cells.

Article Snippet: The recombinant CTRP3 protein (rCTRP3, Catalog Number: CSB-EP883621HU) was commercially procured from Wuhan Cusabio Biotech Co., Ltd. (Hubei, China).

Techniques: Staining, Membrane, Transmission Assay, Electron Microscopy

(A) Representative whole-femur μCT isosurface renderings at 5, 10 and 20dpf for CTRP3 KO, WT and TG mice. Femurs were scanned after removal of intramedullary pins. Apparent bends in 5dpf bones are artifacts of this removal: fractures are straight in vivo. Quantitative callus μCT data for (B) bone volume fraction (BV/TV), (C) bone mineral content (BMC) and (D) bone mineral density (BMD). Solid lines represent p<0.05 by genotype. Maroon up-arrows represent female mice and navy down-arrows represent male mice. For additional quantitative measures of calluses, see Fig S1.

Journal: Journal of orthopaedic research : official publication of the Orthopaedic Research Society

Article Title: CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing

doi: 10.1002/jor.24553

Figure Lengend Snippet: (A) Representative whole-femur μCT isosurface renderings at 5, 10 and 20dpf for CTRP3 KO, WT and TG mice. Femurs were scanned after removal of intramedullary pins. Apparent bends in 5dpf bones are artifacts of this removal: fractures are straight in vivo. Quantitative callus μCT data for (B) bone volume fraction (BV/TV), (C) bone mineral content (BMC) and (D) bone mineral density (BMD). Solid lines represent p<0.05 by genotype. Maroon up-arrows represent female mice and navy down-arrows represent male mice. For additional quantitative measures of calluses, see Fig S1.

Article Snippet: The fracture procedure was then repeated in WT mice aged 34±3 weeks to test a systemic protein delivery strategy; animals in this cohort received either phosphate buffered saline (PBS) vehicle (Vh) or 5.0μg recombinant human CTRP3 (rhCTRP3) (R&D Systems, produced in mouse NS0 cells) in PBS and harvested at 21dpf.

Techniques: In Vivo

Safranin-O micrographs from CTRP3 KO, WT and TG mice at (A) 5dpf, (B) 10dpf and (C) 20dpf. Images are oriented to show one side of the callus in longitudinal section with cortical bone at the bottom (light blue staining). Three selected areas of callus (white squares) are magnified on the right of each panel. For associated histomorphometry, see Fig S2.

Journal: Journal of orthopaedic research : official publication of the Orthopaedic Research Society

Article Title: CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing

doi: 10.1002/jor.24553

Figure Lengend Snippet: Safranin-O micrographs from CTRP3 KO, WT and TG mice at (A) 5dpf, (B) 10dpf and (C) 20dpf. Images are oriented to show one side of the callus in longitudinal section with cortical bone at the bottom (light blue staining). Three selected areas of callus (white squares) are magnified on the right of each panel. For associated histomorphometry, see Fig S2.

Article Snippet: The fracture procedure was then repeated in WT mice aged 34±3 weeks to test a systemic protein delivery strategy; animals in this cohort received either phosphate buffered saline (PBS) vehicle (Vh) or 5.0μg recombinant human CTRP3 (rhCTRP3) (R&D Systems, produced in mouse NS0 cells) in PBS and harvested at 21dpf.

Techniques: Staining

Whole-callus mRNA expression of (A) CTRP3, (B) α-actin-2 (ACTA2), (C) osterix (SP7), (D) collagen-II (COL2A1) and (E) tartrate-resistant acid phosphatase (TRAP) vary based on CTRP3 genotype. Relative expression is presented at 2−dCt with ACTB as a housekeeping gene. Statistics were run on dCt values. Solid lines represent p<0.05 by genotype. Maroon up-arrows represent female mice and navy down-arrows represent male mice.

Journal: Journal of orthopaedic research : official publication of the Orthopaedic Research Society

Article Title: CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing

doi: 10.1002/jor.24553

Figure Lengend Snippet: Whole-callus mRNA expression of (A) CTRP3, (B) α-actin-2 (ACTA2), (C) osterix (SP7), (D) collagen-II (COL2A1) and (E) tartrate-resistant acid phosphatase (TRAP) vary based on CTRP3 genotype. Relative expression is presented at 2−dCt with ACTB as a housekeeping gene. Statistics were run on dCt values. Solid lines represent p<0.05 by genotype. Maroon up-arrows represent female mice and navy down-arrows represent male mice.

Article Snippet: The fracture procedure was then repeated in WT mice aged 34±3 weeks to test a systemic protein delivery strategy; animals in this cohort received either phosphate buffered saline (PBS) vehicle (Vh) or 5.0μg recombinant human CTRP3 (rhCTRP3) (R&D Systems, produced in mouse NS0 cells) in PBS and harvested at 21dpf.

Techniques: Expressing

μCT (A) quantitation and (B) isosurface renderings at 21dpf in mice that received either subcutaneous Vh or 5μg rhCTRP3 protein at time of surgery. Outputs include total volume (TV), bone volume (BV), bone volume fraction (BV/TV), bone mineral content (BMC), bone mineral density (BMD), tissue mineral content (TMC) and tissue mineral density (TMD). Maroon up-arrows represent female mice and navy down-arrows represent male mice.

Journal: Journal of orthopaedic research : official publication of the Orthopaedic Research Society

Article Title: CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing

doi: 10.1002/jor.24553

Figure Lengend Snippet: μCT (A) quantitation and (B) isosurface renderings at 21dpf in mice that received either subcutaneous Vh or 5μg rhCTRP3 protein at time of surgery. Outputs include total volume (TV), bone volume (BV), bone volume fraction (BV/TV), bone mineral content (BMC), bone mineral density (BMD), tissue mineral content (TMC) and tissue mineral density (TMD). Maroon up-arrows represent female mice and navy down-arrows represent male mice.

Article Snippet: The fracture procedure was then repeated in WT mice aged 34±3 weeks to test a systemic protein delivery strategy; animals in this cohort received either phosphate buffered saline (PBS) vehicle (Vh) or 5.0μg recombinant human CTRP3 (rhCTRP3) (R&D Systems, produced in mouse NS0 cells) in PBS and harvested at 21dpf.

Techniques: Quantitation Assay