Ulf Erikssons grupp

Vår forskning undersöker vilken roll vaskulära tillväxtfaktorer spelar i regleringen av blodkärlens stabilitet, lipidbalans och organfunktion. Vi studerar hur dessa faktorer bidrar till tillstånd som ischemisk stroke, diabetisk njursjukdom och metabolt associerad fettleversjukdom (MASLD). Målet är att omsätta våra forskningsresultat i nya och innovativa behandlingsstrategier för kärlrelaterade sjukdomar som påverkar flera olika organ.

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Publikationer

Utvalda publikationer

Finansiering

Forskningsbidrag

  • Förhindrande av trombolys-medierad lipolys för att utvidga behandlingsfönstret för strokepatienter
    Ulla Hamberg Angeby och Lennart Angebys stiftelse
    1 januari 2025 - 31 december 2025
  • European Foundation for the Study of Diabetes
    1 september 2024 - 1 september 2024
  • Swedish Cancer Society
    1 januari 2023
    It is well documented that there is a close link between the onset of cancer and obesity/type 2 diabetes. The connection has been shown for cancer in the liver, pancreas, breast and in the gastrointestinal tract. Whether the cause is linked to high blood sugar or high blood fats is not known. We have developed mouse models to experimentally study the connections between obesity/type 2 diabetes and the onset of liver cancer. Many cancer patients suffer from a form of self-starvation called cachexia. It is not due to a lack of food intake, but the body's tissues break down for unknown reasons. We want to study the mechanisms that cause cachexia in cancer patients. We have developed mouse models to experimentally study the connections between obesity/type 2 diabetes and the onset of liver cancer. In mice fed a special fat-enriched diet, we can study fat accumulation in the liver and how this leads to the development of liver cancer. We have access to drugs that regulate fat accumulation in the liver and we want to study how these can affect the onset of liver cancer. Many cancer patients suffer from a form of self-starvation called cachexia. It is not due to a lack of food intake, but the body's tissues break down for unknown reasons. We want to experimentally study the mechanisms that give rise to cachexia in mouse models. With our research, we hope to increase knowledge about how liver cancer arises due to obesity and type 2 diabetes and how this knowledge can give us new drugs. Obesity and type 2 diabetes are increasing sharply in the population, we hope to be able to develop new forms of preventive treatment for the growing patient groups who are at risk of developing liver cancer. Our research regarding cancer cachexia is to understand the reasons why this serious condition develops in many cancer patients and what can be done to prevent the breakdown of fat and muscle in these patients. The goal is to prevent this 'self-starvation' from developing in cancer patients.
  • Swedish Cancer Society
    1 januari 2020
    It is well documented that there is a close link between the onset of cancer and obesity / type 2 diabetes. The association has been shown for cancer of the liver, pancreas, breasts and gastrointestinal tract. Whether the cause is linked to high blood sugar or high blood fats is not known. We have developed mouse models to experimentally study the associations between obesity / type 2 diabetes and the onset of liver cancer. Many cancer patients suffer from a form of self-starvation called cachexia. It is not due to lack of food intake but the body's tissues are broken down for unknown reasons. We want to study the mechanisms that give rise to cachexia in cancer patients. We have developed mouse models to experimentally study the associations between obesity / type 2 diabetes and the onset of liver cancer. In mice that receive a special fat-enriched diet, we can study fat accumulation in the liver and how this leads to the onset of liver cancer. We have access to drugs that regulate fat accumulation in the liver and we want to study how these can affect the onset of liver cancer. Many cancer patients suffer from a form of self-starvation called cachexia. It is not due to lack of food intake but the body's tissues are broken down for unknown reasons. We want to experimentally study the mechanisms that give rise to cachexia in mouse models. With our research, we hope to increase knowledge about how liver cancer arises due to obesity and type 2 diabetes and how this knowledge can give us new drugs. Given that obesity and type 2 diabetes are increasing sharply in the population, we hope to be able to develop new forms of treatment for the growing patient groups who are at risk of developing liver cancer. Our research on cancer cachexia is to understand the reasons why this serious condition develops and how to do to prevent the breakdown of fat and muscle in these patients.
  • Metabolic aspects of cancer development and treatment with a focus on liver cancer and cachexia
    Swedish Cancer Society
    1 januari 2019
    It is well documented that there is a close link between the onset of cancer and obesity / type 2 diabetes. The association has been shown for cancer of the liver, pancreas, breasts and gastrointestinal tract. Whether the cause is linked to high blood sugar or high blood fats is not known. We have developed mouse models to experimentally study the associations between obesity / type 2 diabetes and the onset of liver cancer. Many cancer patients suffer from a form of self-starvation called cachexia. It is not due to lack of food intake but the body's tissues are broken down for unknown reasons. We want to study the mechanisms that give rise to cachexia in cancer patients. We have developed mouse models to experimentally study the associations between obesity / type 2 diabetes and the onset of liver cancer. In mice that receive a special fat-enriched diet, we can study fat accumulation in the liver and how this leads to the onset of liver cancer. We have access to drugs that regulate fat accumulation in the liver and we want to study how these can affect the onset of liver cancer. Many cancer patients suffer from a form of self-starvation called cachexia. It is not due to lack of food intake but the body's tissues are broken down for unknown reasons. We want to experimentally study the mechanisms that give rise to cachexia in mouse models. With our research, we hope to increase knowledge about how liver cancer arises due to obesity and type 2 diabetes and how this knowledge can give us new drugs. Given that obesity and type 2 diabetes are increasing sharply in the population, we hope to be able to develop new forms of treatment for the growing patient groups who are at risk of developing liver cancer. Our research on cancer cachexia is to understand the reasons why this serious condition develops and how to do to prevent the breakdown of fat and muscle in these patients.
  • Role of VEGF-B i diabetic complications
    Novo Nordisk Foundation
    1 januari 2018 - 1 januari 2021
  • Metabolic aspects of the onset and treatment of cancer with a focus on liver cancer and cachexia
    Swedish Cancer Society
    1 januari 2018
    It has been established that the development of liver cancer is closely associated with excessive calorie intake, obesity, the metabolic syndrome and the onset of type 2 diabetes. We want to investigate whether reducing the incidence of fat in liver in obese individuals can reduce the appearance of liver cancer. Many cancer patients suffer from a form of starvation symptoms during diseases called cachexia. This leads to muscle wasting, fatigue, severe reduction in quality of life, and impaired ability to be treated with certain cancer drugs. We want to investigate how the nutrient uptake from the blood vessels to the body's various tissues works at cachexia. Cancer research today often focuses on the genetic or other cause of the onset of cancer. There is less focus on the risks that one can influence through a healthy life. Obesity and type 2 diabetes lead to a greatly increased risk of developing cancer. We want to investigate how to reduce the development of liver cancer in obese and diabetic individuals by studying the corresponding mouse models. Furthermore, we want to understand how cancer patients with a form of self-starvation, who break down the muscles, called cachexia, can be offered a treatment that reduces the suffering in this sequelae of the cancer. Our research aims to investigate whether liver cancer can occur in patients with obesity, metabolic syndrome and type 2 diabetes by reducing morbid fat accumulation in the liver. Furthermore, we want to investigate why cancer patients with starvation cachexia do not get enough nutrition for their tissues and we will
  • Swedish Research Council
    1 januari 2018 - 31 december 2027
    Most human disease have a direct or indirect involvement with the vascular system in the body, and in many cases have an inadequate function of the vasculature has a direct role in morbidity and mortality of affected patients. An example is cardiovascular disease where the malfunction of the vasculature is a direct cause of the disease. Therefore, understanding the role of the vasculature in normal human physiology and human disease is of outmost importance.The inner  lining of blood vessels, the endothelium, is the specialized interface between the blood stream and the organ parenchyma. The function of the endothelium in different organs is optimized to serve the physiological needs of the organ parenchyme and the specialization can be observed on both the structural level with continous, fenestrated and discontinous endothelium, as well as on the level of specifically expressed genes in endothelial cells in diferent vascular beds.In my research I focus on two different growth factor and how these factor in a paracrine fashion instructs the endothelium to serve tissue specific functions in different vascular beds. The focus is on VEGF-B and its role endothelial transcytosis of fatty acids, steatosis and in type 2 diabetes and its complications. I am also focusing on PDGF-C and its role on controlling the integrity and function of the blood-brain barrier under normal conditions and in CNS trauma, in particular in ischemic stroke.
  • Role of VEGF-B signaling in diabetic complications
    Novo Nordisk Foundation
    1 januari 2017 - 1 januari 2018
  • Metabolic aspects of the onset and treatment of cancer with a focus on liver cancer and cachexia
    Swedish Cancer Society
    1 januari 2017
    It has been established that the development of liver cancer is closely associated with excessive calorie intake, obesity, the metabolic syndrome and the onset of type 2 diabetes. We want to investigate whether reducing the incidence of fat in liver in obese individuals can reduce the appearance of liver cancer. Many cancer patients suffer from a form of starvation symptoms during diseases called cachexia. This leads to muscle wasting, fatigue, severe reduction in quality of life, and impaired ability to be treated with certain cancer drugs. We want to investigate how the nutrient uptake from the blood vessels to the body's various tissues works at cachexia. Cancer research today often focuses on the genetic or other cause of the onset of cancer. There is less focus on the risks that one can influence through a healthy life. Obesity and type 2 diabetes lead to a greatly increased risk of developing cancer. We want to investigate how to reduce the development of liver cancer in obese and diabetic individuals by studying the corresponding mouse models. Furthermore, we want to understand how cancer patients with a form of self-starvation, who break down the muscles, called cachexia, can be offered a treatment that reduces the suffering in this sequelae of the cancer. Our research aims to investigate whether liver cancer can occur in patients with obesity, metabolic syndrome and type 2 diabetes by reducing morbid fat accumulation in the liver. Furthermore, we want to investigate why cancer patients with starvation cachexia do not get enough nutrition for their tissues and we will
  • Swedish Research Council
    1 januari 2017 - 31 december 2017
  • Swedish Research Council
    1 januari 2017 - 31 december 2020
  • Metabolic aspects of the onset and treatment of cancer with a focus on liver cancer and cachexia
    Swedish Cancer Society
    1 januari 2016
    It has been established that the development of liver cancer is closely associated with excessive calorie intake, obesity, the metabolic syndrome and the onset of type 2 diabetes. We want to investigate whether reducing the incidence of fat in liver in obese individuals can reduce the appearance of liver cancer. Many cancer patients suffer from a form of starvation symptoms during diseases called cachexia. This leads to muscle wasting, fatigue, severe reduction in quality of life, and impaired ability to be treated with certain cancer drugs. We want to investigate how the nutrient uptake from the blood vessels to the body's various tissues works at cachexia. Cancer research today often focuses on the genetic or other cause of the onset of cancer. There is less focus on the risks that one can influence through a healthy life. Obesity and type 2 diabetes lead to a greatly increased risk of developing cancer. We want to investigate how to reduce the development of liver cancer in obese and diabetic individuals by studying the corresponding mouse models. Furthermore, we want to understand how cancer patients with a form of self-starvation, who break down the muscles, called cachexia, can be offered a treatment that reduces the suffering in this sequelae of the cancer. Our research aims to investigate whether liver cancer can occur in patients with obesity, metabolic syndrome and type 2 diabetes by reducing morbid fat accumulation in the liver. Furthermore, we want to investigate why cancer patients with starvation cachexia do not get enough nutrition for their tissues and we will
  • Importance of some growth factors in tumor biology, with particular focus on members of the VEGF / PDGF family
    Swedish Cancer Society
    1 januari 2015
    All solid tumors consist of a mixture of tumor cells and normal cells, the so-called tumor tumor. Tumor metabolism consists of fibroblasts, inflammatory cells, and blood vessel cells. Tumor metabolism plays an important role when the tumor cells grow and spread. For example, the blood vessels must grow in step with the tumor, as the tumor otherwise dies of oxygen and nutrient deficiency. The reason why tumor tumors grow in step with the tumor is that tumor cells emit various types of growth factors, which stimulate the normal cells to migrate into the tumor and thus stimulate the tumor cells. own growth. The emergence of tumors also often results in tissue edema. This research project is about studying basic mechanisms that regulate how tumors grow and spread. Growth factors, a group of body proteins, have a crucial importance here. We also intend to develop and use monoclonal antibodies, which enable us to neutralize the effects of these factors. Increased knowledge of the signals that tumor cells use to direct normal cells into tumors, to form the necessary scans. tumor tomato may result in alternative treatment options. Furthermore, we want to study a mechanism that regulates edema formation in nerve tissue and possibly. also in tumors of the brain. We hope to show that a number of growth factors we isolated have an important role in tumor biology. We have developed monoclonal antibodies to these to be able to neutralize these factors in different tumor models and we now want to take another step by studying these factors in human tumors. We have also discovered a new mechanism for how cells, including tumor cells, obtain some necessary nutrients from the blood. Blocking this mechanism may affect tumor growth. We identified a new mechanism for how edema occurs in nerve tissue and this mechanism may have significance for how tumors in the brain should be treated.
  • Importance of some growth factors in tumor biology, with particular focus on members of the VEGF / PDGF family
    Swedish Cancer Society
    1 januari 2014
    All solid tumors consist of a mixture of tumor cells and normal cells, the so-called tumor tumor. Tumor metabolism consists of fibroblasts, inflammatory cells, and blood vessel cells. Tumor metabolism plays an important role when the tumor cells grow and spread. For example, the blood vessels must grow in step with the tumor, as the tumor otherwise dies of oxygen and nutrient deficiency. The reason why tumor tumors grow in step with the tumor is that tumor cells emit various types of growth factors, which stimulate the normal cells to migrate into the tumor and thus stimulate the tumor cells. own growth. The emergence of tumors also often results in tissue edema. This research project is about studying basic mechanisms that regulate how tumors grow and spread. Growth factors, a group of body proteins, have a crucial importance here. We also intend to develop and use monoclonal antibodies, which enable us to neutralize the effects of these factors. Increased knowledge of the signals that tumor cells use to direct normal cells into tumors, to form the necessary scans. tumor tomato may result in alternative treatment options. Furthermore, we want to study a mechanism that regulates edema formation in nerve tissue and possibly. also in tumors of the brain. We hope to show that a number of growth factors we isolated have an important role in tumor biology. We have developed monoclonal antibodies to these to be able to neutralize these factors in different tumor models and we now want to take another step by studying these factors in human tumors. We have also discovered a new mechanism for how cells, including tumor cells, obtain some necessary nutrients from the blood. Blocking this mechanism may affect tumor growth. We identified a new mechanism for how edema occurs in nerve tissue and this mechanism may have significance for how tumors in the brain should be treated.
  • Swedish Research Council
    1 januari 2013 - 31 december 2015
  • Swedish Research Council
    1 januari 2012 - 31 december 2016
  • VINNOVA
    1 december 2011 - 31 december 2016
  • VINNOVA
    1 juli 2009 - 30 november 2014
  • Swedish Research Council
    1 januari 2009 - 31 december 2011
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