Overview
SCIENTIFIC SCORE
Moderately Effective
Based on 7 Researches
8
USERS' SCORE
Good
Based on 6 Reviews
8
Supplement Facts
Serving Size: About 1/4 cup (31 g)
Amount Per Serving
%DV
Calories
180
Total Fat
13 g
17%
Saturated Fat
3 g
15%
Trans Fat
0 g
Cholesterol
0 mg
0%
Sodium
0 mg
0%
Total Carbohydrate
4 g
1%
Dietary Fiber
2 g
7%
Total Sugars
0 g
Includes 0g Added Sugars
0%
Protein
11g
Vit. D
0 mcg
0%
Calcium
8 mg
0%
Iron
4 mg
20%
Potassium
243 mg
6%
Top Medical Research Studies
9
We aimed to uncover how the proteins VEGFA and bFGF can support heart recovery following a heart attack, and we did this by enhancing human adipose-derived stem cells (hADSCs) with modified mRNA. These proteins are known to play a role in improving blood flow and reducing cell death, both vital for effective healing.
By modifying the hADSCs to overexpress these proteins, we sought to improve their ability to support the heart during such a critical time. Importantly, our approach involved using a new technique that enables the hADSCs to produce these growth factors in a timed, efficient manner. This modification not only led to better survival of the transplanted cells but also promoted stable formation of new blood vessels at the site of injury.
We observed that the infused hADSCs improved overall heart function and electrical activity, suggesting a robust response to the proteins we introduced. The results indicate that the combination of these engineered stem cells and the proteins could substantially enhance recovery after a heart attack, paving the way for new treatments for heart diseases caused by ischemia.
By modifying the hADSCs to overexpress these proteins, we sought to improve their ability to support the heart during such a critical time. Importantly, our approach involved using a new technique that enables the hADSCs to produce these growth factors in a timed, efficient manner. This modification not only led to better survival of the transplanted cells but also promoted stable formation of new blood vessels at the site of injury.
We observed that the infused hADSCs improved overall heart function and electrical activity, suggesting a robust response to the proteins we introduced. The results indicate that the combination of these engineered stem cells and the proteins could substantially enhance recovery after a heart attack, paving the way for new treatments for heart diseases caused by ischemia.
Read More
8
We focused on understanding how certain proteins can influence the healing process of heart cells after a heart attack, specifically looking at the role of circALPK2, a circular RNA that seems to control the growth of these cells.
Our research used cardiomyocytes, the heart cells derived from human embryonic stem cells, to analyze the behavior of circALPK2. By silencing circALPK2 using a specific technique, we examined how this affected cell growth and regeneration.
Interestingly, we discovered that knocking down circALPK2 enhanced the proliferation of these cardiomyocytes. This means that removing the influence of circALPK2 allowed heart cells to multiply more effectively, which could be crucial for repairing damage after a myocardial infarction.
Moreover, we identified a specific interaction between circALPK2, a microRNA, and a target protein called GSK3B that plays a significant role in cell growth. This finding opens the door to potential new therapies that could improve heart recovery by focusing on this molecular pathway.
Our research used cardiomyocytes, the heart cells derived from human embryonic stem cells, to analyze the behavior of circALPK2. By silencing circALPK2 using a specific technique, we examined how this affected cell growth and regeneration.
Interestingly, we discovered that knocking down circALPK2 enhanced the proliferation of these cardiomyocytes. This means that removing the influence of circALPK2 allowed heart cells to multiply more effectively, which could be crucial for repairing damage after a myocardial infarction.
Moreover, we identified a specific interaction between circALPK2, a microRNA, and a target protein called GSK3B that plays a significant role in cell growth. This finding opens the door to potential new therapies that could improve heart recovery by focusing on this molecular pathway.
Read More
8
We investigated how the proteins CELF1 and FMO2 influence heart remodeling after a heart attack, particularly focusing on how they might affect recovery processes. Our study involved inducing heart attacks in mice and then manipulating the expression levels of these proteins to observe their effects.
By silencing CELF1, we noted an increase in FMO2 levels, which was linked to improved heart function and reduced heart damage. We observed that the typical outcomes of a heart attack, such as myocardial fibrosis and ECM deposition, were alleviated. Yet, when we tried boosting FMO2 through a different method, the results led to improvements in heart structure and function, suggesting FMO2’s significant role in healing after heart attacks.
Ultimately, our findings suggest that CELF1 promotes adverse heart remodeling following a heart attack by inhibiting FMO2. Therefore, targeting this pathway may offer new avenues for treatment and recovery in heart attack patients. We believe these insights could pave the way for more effective therapies in the future.
By silencing CELF1, we noted an increase in FMO2 levels, which was linked to improved heart function and reduced heart damage. We observed that the typical outcomes of a heart attack, such as myocardial fibrosis and ECM deposition, were alleviated. Yet, when we tried boosting FMO2 through a different method, the results led to improvements in heart structure and function, suggesting FMO2’s significant role in healing after heart attacks.
Ultimately, our findings suggest that CELF1 promotes adverse heart remodeling following a heart attack by inhibiting FMO2. Therefore, targeting this pathway may offer new avenues for treatment and recovery in heart attack patients. We believe these insights could pave the way for more effective therapies in the future.
Read More
Most Useful Reviews
8
Promotes heart health
Excellent product! Pumpkin seeds are a delightful, crunchy snack that enhances my diet. They offer many health benefits, including heart health and digestion improvement. I recommend them for their rich nutrients and great taste.
Read More
7.5
Reduces heart attack risk
Excellent! The high magnesium content in pumpkin seeds helps reduce the risk of heart attacks, maintain normal blood pressure, lower blood sugar levels, and support healthy bone formation.
Read More
7.5
Heart health boost
Amazing! This high-quality, crunchy product is affordable. Pumpkin seeds are nutrient-rich, supporting blood sugar maintenance, fertility, and heart health. I add them to cereals, salads, or enjoy them as a snack at work, which my colleagues love too.
Read More
Medical Researches
SCIENTIFIC SCORE
Moderately Effective
Based on 7 Researches
8
- All Researches
9
We explored the potential of TAPI-1, a protein that inhibits harmful enzymes, in treating heart damage after a heart attack, using a novel delivery method. To enhance its effectiveness, researchers created nanoparticles that mimic neutrophils, a type of immune cell that quickly appears in injured heart tissue.
These specialized nanoparticles were loaded with TAPI-1 and specifically designed to target inflamed areas of the heart in rats following a heart attack. By delivering TAPI-1 more precisely, we aimed to reduce heart injury and improve heart function.
Our results were promising—injecting TAPI-1 through these neutrophil-mimicking nanoparticles led to better heart performance and less scar tissue compared to standard TAPI-1 treatments. Not only did the targeted approach seem to optimize the protein's effects, but it also helped lessen the overall inflammation within the heart.
In summary, this study highlights a strategic advancement in delivering the TAPI-1 protein that could lead to more effective treatments for heart attack recovery, ultimately improving patient outcomes.
These specialized nanoparticles were loaded with TAPI-1 and specifically designed to target inflamed areas of the heart in rats following a heart attack. By delivering TAPI-1 more precisely, we aimed to reduce heart injury and improve heart function.
Our results were promising—injecting TAPI-1 through these neutrophil-mimicking nanoparticles led to better heart performance and less scar tissue compared to standard TAPI-1 treatments. Not only did the targeted approach seem to optimize the protein's effects, but it also helped lessen the overall inflammation within the heart.
In summary, this study highlights a strategic advancement in delivering the TAPI-1 protein that could lead to more effective treatments for heart attack recovery, ultimately improving patient outcomes.
Read More
9
We aimed to uncover how the proteins VEGFA and bFGF can support heart recovery following a heart attack, and we did this by enhancing human adipose-derived stem cells (hADSCs) with modified mRNA. These proteins are known to play a role in improving blood flow and reducing cell death, both vital for effective healing.
By modifying the hADSCs to overexpress these proteins, we sought to improve their ability to support the heart during such a critical time. Importantly, our approach involved using a new technique that enables the hADSCs to produce these growth factors in a timed, efficient manner. This modification not only led to better survival of the transplanted cells but also promoted stable formation of new blood vessels at the site of injury.
We observed that the infused hADSCs improved overall heart function and electrical activity, suggesting a robust response to the proteins we introduced. The results indicate that the combination of these engineered stem cells and the proteins could substantially enhance recovery after a heart attack, paving the way for new treatments for heart diseases caused by ischemia.
By modifying the hADSCs to overexpress these proteins, we sought to improve their ability to support the heart during such a critical time. Importantly, our approach involved using a new technique that enables the hADSCs to produce these growth factors in a timed, efficient manner. This modification not only led to better survival of the transplanted cells but also promoted stable formation of new blood vessels at the site of injury.
We observed that the infused hADSCs improved overall heart function and electrical activity, suggesting a robust response to the proteins we introduced. The results indicate that the combination of these engineered stem cells and the proteins could substantially enhance recovery after a heart attack, paving the way for new treatments for heart diseases caused by ischemia.
Read More
8
We focused on understanding how certain proteins can influence the healing process of heart cells after a heart attack, specifically looking at the role of circALPK2, a circular RNA that seems to control the growth of these cells.
Our research used cardiomyocytes, the heart cells derived from human embryonic stem cells, to analyze the behavior of circALPK2. By silencing circALPK2 using a specific technique, we examined how this affected cell growth and regeneration.
Interestingly, we discovered that knocking down circALPK2 enhanced the proliferation of these cardiomyocytes. This means that removing the influence of circALPK2 allowed heart cells to multiply more effectively, which could be crucial for repairing damage after a myocardial infarction.
Moreover, we identified a specific interaction between circALPK2, a microRNA, and a target protein called GSK3B that plays a significant role in cell growth. This finding opens the door to potential new therapies that could improve heart recovery by focusing on this molecular pathway.
Our research used cardiomyocytes, the heart cells derived from human embryonic stem cells, to analyze the behavior of circALPK2. By silencing circALPK2 using a specific technique, we examined how this affected cell growth and regeneration.
Interestingly, we discovered that knocking down circALPK2 enhanced the proliferation of these cardiomyocytes. This means that removing the influence of circALPK2 allowed heart cells to multiply more effectively, which could be crucial for repairing damage after a myocardial infarction.
Moreover, we identified a specific interaction between circALPK2, a microRNA, and a target protein called GSK3B that plays a significant role in cell growth. This finding opens the door to potential new therapies that could improve heart recovery by focusing on this molecular pathway.
Read More
8
We investigated how the proteins CELF1 and FMO2 influence heart remodeling after a heart attack, particularly focusing on how they might affect recovery processes. Our study involved inducing heart attacks in mice and then manipulating the expression levels of these proteins to observe their effects.
By silencing CELF1, we noted an increase in FMO2 levels, which was linked to improved heart function and reduced heart damage. We observed that the typical outcomes of a heart attack, such as myocardial fibrosis and ECM deposition, were alleviated. Yet, when we tried boosting FMO2 through a different method, the results led to improvements in heart structure and function, suggesting FMO2’s significant role in healing after heart attacks.
Ultimately, our findings suggest that CELF1 promotes adverse heart remodeling following a heart attack by inhibiting FMO2. Therefore, targeting this pathway may offer new avenues for treatment and recovery in heart attack patients. We believe these insights could pave the way for more effective therapies in the future.
By silencing CELF1, we noted an increase in FMO2 levels, which was linked to improved heart function and reduced heart damage. We observed that the typical outcomes of a heart attack, such as myocardial fibrosis and ECM deposition, were alleviated. Yet, when we tried boosting FMO2 through a different method, the results led to improvements in heart structure and function, suggesting FMO2’s significant role in healing after heart attacks.
Ultimately, our findings suggest that CELF1 promotes adverse heart remodeling following a heart attack by inhibiting FMO2. Therefore, targeting this pathway may offer new avenues for treatment and recovery in heart attack patients. We believe these insights could pave the way for more effective therapies in the future.
Read More
8
We utilized advanced Olink cardiovascular metabolomics technology to delve into protein biomarkers linked to acute myocardial infarction (AMI), a serious heart condition caused by sudden blood flow interruption. By analyzing blood samples from 20 AMI patients and 10 healthy controls, we identified proteins that showed different expressions connected to this life-threatening event.
After pinpointing these proteins, we enhanced our investigation by studying a larger group, including 125 AMI patients and 120 healthy controls, to validate the findings. We focused on five core proteins—PCOLCE, FCN2, REG1A, DEFA1, and CRTAC1—that emerged as promising candidates for early diagnosis and risk assessment of AMI.
Our findings suggest these proteins could be pivotal in developing targeted treatments to reduce cardiovascular damage during heart attacks. While we are optimistic about these potential biomarkers, it’s important to note that we did not directly evaluate their effects in treatment settings just yet.
After pinpointing these proteins, we enhanced our investigation by studying a larger group, including 125 AMI patients and 120 healthy controls, to validate the findings. We focused on five core proteins—PCOLCE, FCN2, REG1A, DEFA1, and CRTAC1—that emerged as promising candidates for early diagnosis and risk assessment of AMI.
Our findings suggest these proteins could be pivotal in developing targeted treatments to reduce cardiovascular damage during heart attacks. While we are optimistic about these potential biomarkers, it’s important to note that we did not directly evaluate their effects in treatment settings just yet.
Read More
User Reviews
USERS' SCORE
Good
Based on 6 Reviews
8
- All Reviews
- Positive Reviews
- Negative Reviews
8
Promotes heart health
Excellent product! Pumpkin seeds are a delightful, crunchy snack that enhances my diet. They offer many health benefits, including heart health and digestion improvement. I recommend them for their rich nutrients and great taste.
Read More
7.5
Reduces heart attack risk
Excellent! The high magnesium content in pumpkin seeds helps reduce the risk of heart attacks, maintain normal blood pressure, lower blood sugar levels, and support healthy bone formation.
Read More
7.5
Heart health boost
Amazing! This high-quality, crunchy product is affordable. Pumpkin seeds are nutrient-rich, supporting blood sugar maintenance, fertility, and heart health. I add them to cereals, salads, or enjoy them as a snack at work, which my colleagues love too.
Read More
7.5
Aids heart health
Upon my nutritionist's recommendation, I discovered pumpkin seeds on iHerb. They support heart health, lower blood sugar, and improve male reproductive functions. They are also excellent as a snack or in salads.
Read More
6
Improves heart health
The product quality is excellent—clean, abundant, and sweet-tasting. These pumpkin seeds are powerhouses of nutrition, offering numerous health benefits, including enhancing heart health and preventing certain cancers. I consume a handful daily; this is my second purchase!
Read More
Frequently Asked Questions
7.5
Reduces heart attack risk
Excellent! The high magnesium content in pumpkin seeds helps reduce the risk of heart attacks, maintain normal blood pressure, lower blood sugar levels, and support healthy bone formation.
6
Supports heart function
Discovering the benefits of pumpkin seeds led me to incorporate them into my meals. They are delicious and beneficial for the heart and regulating blood sugar. Consuming them daily contributes to good health, and the quality is excellent.
6
Improves heart health
The product quality is excellent—clean, abundant, and sweet-tasting. These pumpkin seeds are powerhouses of nutrition, offering numerous health benefits, including enhancing heart health and preventing certain cancers. I consume a handful daily; this is my second purchase!
8
Promotes heart health
Excellent product! Pumpkin seeds are a delightful, crunchy snack that enhances my diet. They offer many health benefits, including heart health and digestion improvement. I recommend them for their rich nutrients and great taste.
7.5
Heart health boost
Amazing! This high-quality, crunchy product is affordable. Pumpkin seeds are nutrient-rich, supporting blood sugar maintenance, fertility, and heart health. I add them to cereals, salads, or enjoy them as a snack at work, which my colleagues love too.
7.5
Aids heart health
Upon my nutritionist's recommendation, I discovered pumpkin seeds on iHerb. They support heart health, lower blood sugar, and improve male reproductive functions. They are also excellent as a snack or in salads.
9
We explored the potential of TAPI-1, a protein that inhibits harmful enzymes, in treating heart damage after a heart attack, using a novel delivery method. To enhance its effectiveness, researchers created nanoparticles that mimic neutrophils, a type of immune cell that quickly appears in injured heart tissue.
These specialized nanoparticles were loaded with TAPI-1 and specifically designed to target inflamed areas of the heart in rats following a heart attack. By delivering TAPI-1 more precisely, we aimed to reduce heart injury and improve heart function.
Our results were promising—injecting TAPI-1 through these neutrophil-mimicking nanoparticles led to better heart performance and less scar tissue compared to standard TAPI-1 treatments. Not only did the targeted approach seem to optimize the protein's effects, but it also helped lessen the overall inflammation within the heart.
In summary, this study highlights a strategic advancement in delivering the TAPI-1 protein that could lead to more effective treatments for heart attack recovery, ultimately improving patient outcomes.
These specialized nanoparticles were loaded with TAPI-1 and specifically designed to target inflamed areas of the heart in rats following a heart attack. By delivering TAPI-1 more precisely, we aimed to reduce heart injury and improve heart function.
Our results were promising—injecting TAPI-1 through these neutrophil-mimicking nanoparticles led to better heart performance and less scar tissue compared to standard TAPI-1 treatments. Not only did the targeted approach seem to optimize the protein's effects, but it also helped lessen the overall inflammation within the heart.
In summary, this study highlights a strategic advancement in delivering the TAPI-1 protein that could lead to more effective treatments for heart attack recovery, ultimately improving patient outcomes.
8
We focused on understanding how certain proteins can influence the healing process of heart cells after a heart attack, specifically looking at the role of circALPK2, a circular RNA that seems to control the growth of these cells.
Our research used cardiomyocytes, the heart cells derived from human embryonic stem cells, to analyze the behavior of circALPK2. By silencing circALPK2 using a specific technique, we examined how this affected cell growth and regeneration.
Interestingly, we discovered that knocking down circALPK2 enhanced the proliferation of these cardiomyocytes. This means that removing the influence of circALPK2 allowed heart cells to multiply more effectively, which could be crucial for repairing damage after a myocardial infarction.
Moreover, we identified a specific interaction between circALPK2, a microRNA, and a target protein called GSK3B that plays a significant role in cell growth. This finding opens the door to potential new therapies that could improve heart recovery by focusing on this molecular pathway.
Our research used cardiomyocytes, the heart cells derived from human embryonic stem cells, to analyze the behavior of circALPK2. By silencing circALPK2 using a specific technique, we examined how this affected cell growth and regeneration.
Interestingly, we discovered that knocking down circALPK2 enhanced the proliferation of these cardiomyocytes. This means that removing the influence of circALPK2 allowed heart cells to multiply more effectively, which could be crucial for repairing damage after a myocardial infarction.
Moreover, we identified a specific interaction between circALPK2, a microRNA, and a target protein called GSK3B that plays a significant role in cell growth. This finding opens the door to potential new therapies that could improve heart recovery by focusing on this molecular pathway.
8
We investigated how the proteins CELF1 and FMO2 influence heart remodeling after a heart attack, particularly focusing on how they might affect recovery processes. Our study involved inducing heart attacks in mice and then manipulating the expression levels of these proteins to observe their effects.
By silencing CELF1, we noted an increase in FMO2 levels, which was linked to improved heart function and reduced heart damage. We observed that the typical outcomes of a heart attack, such as myocardial fibrosis and ECM deposition, were alleviated. Yet, when we tried boosting FMO2 through a different method, the results led to improvements in heart structure and function, suggesting FMO2’s significant role in healing after heart attacks.
Ultimately, our findings suggest that CELF1 promotes adverse heart remodeling following a heart attack by inhibiting FMO2. Therefore, targeting this pathway may offer new avenues for treatment and recovery in heart attack patients. We believe these insights could pave the way for more effective therapies in the future.
By silencing CELF1, we noted an increase in FMO2 levels, which was linked to improved heart function and reduced heart damage. We observed that the typical outcomes of a heart attack, such as myocardial fibrosis and ECM deposition, were alleviated. Yet, when we tried boosting FMO2 through a different method, the results led to improvements in heart structure and function, suggesting FMO2’s significant role in healing after heart attacks.
Ultimately, our findings suggest that CELF1 promotes adverse heart remodeling following a heart attack by inhibiting FMO2. Therefore, targeting this pathway may offer new avenues for treatment and recovery in heart attack patients. We believe these insights could pave the way for more effective therapies in the future.
We conducted a double-blinded, placebo-controlled clinical trial to investigate how colchicine—a drug known for its anti-inflammatory properties—affects patients after an acute myocardial infarction (AMI), commonly known as a heart attack. Our study included 161 eligible participants from three hospitals in East Java, Indonesia, where they were randomly assigned to receive either colchicine or standard treatment over a 30-day period.
Throughout the trial, we measured key inflammatory markers and cardiac health indicators. While colchicine did lower NT-proBNP, a protein associated with heart failure, and also significantly reduced levels of Caspase-1, TGF-β, and Galectin-3—markers indicating inflammation and fibrosis—there was no notable improvement in echocardiography parameters measuring heart function.
This finding illustrates that while colchicine may help reduce certain inflammatory responses following a heart attack, it did not lead to measurable improvements in heart function as assessed through echocardiography. Thus, we conclude that the effects of colchicine could be beneficial for mitigating inflammation post-AMI, but it does not significantly enhance cardiac function in the short term.
Throughout the trial, we measured key inflammatory markers and cardiac health indicators. While colchicine did lower NT-proBNP, a protein associated with heart failure, and also significantly reduced levels of Caspase-1, TGF-β, and Galectin-3—markers indicating inflammation and fibrosis—there was no notable improvement in echocardiography parameters measuring heart function.
This finding illustrates that while colchicine may help reduce certain inflammatory responses following a heart attack, it did not lead to measurable improvements in heart function as assessed through echocardiography. Thus, we conclude that the effects of colchicine could be beneficial for mitigating inflammation post-AMI, but it does not significantly enhance cardiac function in the short term.
References
- Chen Q, Yu Y, Tong L, Weiss RM, Wei SG. Targeted delivery of TAPI-1 via biomimetic nanoparticles ameliorates post-infarct left ventricle function and remodeling. Cardiovasc Res. 2025. 10.1093/cvr/cvaf039
- Wu H, Jiang X, Fan H, Li J, Li Y, et al. Inhibition of circALPK2 enhances proliferation and therapeutic potential of human pluripotent stem cell-derived cardiomyocytes in myocardial infarction. Stem Cell Res Ther. 2025;16:107. 10.1186/s13287-025-04230-8
- Lai J, Li L, Liu J, Yan Q, Xu Z, et al. CELF1 Promotes Post-myocardial Infarction Cardiac Remodeling Via Suppression of FMO2. Cardiovasc Toxicol. 2025;25:441. 10.1007/s12012-024-09951-5
- Stephan JK, Knerr T, Gu Z, Li H, Brittian KR, et al. Neutrophil-secreted CHI3L1 exacerbates cardiac dysfunction and inflammation after myocardial infarction. FASEB J. 2025;39:e70422. 10.1096/fj.202401654R
- Tan X, Wang X, Xu S, Zeng Y, Zhang G, et al. Identification of Cardiometabolic Protein Biomarkers for Acute Myocardial Infarction Using Olink Proteomics. J Inflamm Res. 2025;18:2629. 10.2147/JIR.S495784
- Li K, Luo R, Yu X, Dong W, Hao G, et al. Enhanced human adipose-derived stem cells with VEGFA and bFGF mRNA promote stable vascular regeneration and improve cardiac function following myocardial infarction. Clin Transl Med. 2025;15:e70250. 10.1002/ctm2.70250
- Astiawati T, Rohman MS, Wihastuti T, Sujuti H, Endharti AT, et al. Efficacy of Colchicine in Reducing NT-proBNP, Caspase-1, TGF-β, and Galectin-3 Expression and Improving Echocardiography Parameters in Acute Myocardial Infarction: A Multi-Center, Randomized, Placebo-Controlled, Double-Blinded Clinical Trial. J Clin Med. 2025;14. 10.3390/jcm14041347
