scholarly journals C1q Complement/Tumor Necrosis Factor-Associated Proteins in Cardiovascular Disease and COVID-19

Proteomes ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 12
Author(s):  
Yaoli Xie ◽  
Zhijun Meng ◽  
Jia Gao ◽  
Caihong Liu ◽  
Jing Wang ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Tumor Necrosis Factor ◽  
Cardiovascular System ◽  
Tumor Necrosis ◽  
Current Knowledge ◽  
Immune Surveillance ◽  
Treatment Strategies ◽  
Cardiovascular Complications ◽  
Associated Proteins ◽  
Necrosis Factor

With continually improving treatment strategies and patient care, the overall mortality of cardiovascular disease (CVD) has been significantly reduced. However, this success is a double-edged sword, as many patients who survive cardiovascular complications will progress towards a chronic disorder over time. A family of adiponectin paralogs designated as C1q complement/tumor necrosis factor (TNF)-associated proteins (CTRPs) has been found to play a role in the development of CVD. CTRPs, which are comprised of 15 members, CTRP1 to CTRP15, are secreted from different organs/tissues and exhibit diverse functions, have attracted increasing attention because of their roles in maintaining inner homeostasis by regulating metabolism, inflammation, and immune surveillance. In particular, studies indicate that CTRPs participate in the progression of CVD, influencing its prognosis. This review aims to improve understanding of the role of CTRPs in the cardiovascular system by analyzing current knowledge. In particular, we examine the association of CTRPs with endothelial cell dysfunction, inflammation, and diabetes, which are the basis for development of CVD. Additionally, the recently emerged novel coronavirus (COVID-19), officially known as severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has been found to trigger severe cardiovascular injury in some patients, and evidence indicates that the mortality of COVID-19 is much higher in patients with CVD than without CVD. Understanding the relationship of CTRPs and the SARS-CoV-2-related damage to the cardiovascular system, as well as the potential mechanisms, will achieve a profound insight into a therapeutic strategy to effectively control CVD and reduce the mortality rate.

Emerging Applications of the Tumor Necrosis Factor Family of Ligands and Receptors in Cancer Therapy

2003 ◽  
Vol 21 (18) ◽  
pp. 3526-3534 ◽  
Author(s):  
Anas Younes ◽  
Marshall E. Kadin
Keyword(s):  
Tumor Necrosis Factor ◽  
Mammalian Cells ◽  
Tumor Necrosis ◽  
Family Members ◽  
Treatment Strategies ◽  
Cd40 Ligand ◽  
Nuclear Factor Κb ◽  
Trail Receptors ◽  
Novel Treatment Strategies ◽  
Necrosis Factor

Abnormalities of the tumor necrosis factor (TNF) family members have been linked to several human diseases, including cancer. Novel treatment strategies for cancer are emerging based on an understanding of the function of TNF family members. The advantage of these strategies is their potential to selectively target cancer cells, while sparing normal cells. Combining these new strategies with currently available treatments such as chemotherapy and radiation therapy is under investigation, with promising results. However, because some TNF family members are toxic to normal mammalian cells when administered systemically, only a few TNF family members have potential therapeutic value. This concise review focuses on the clinical implications of four TNF family members for cancer treatment: CD30/CD30 ligand, CD40/CD40 ligand, receptor activator of nuclear factor-κB (RANK)/RANK ligand, and TNF-related apoptosis-inducing ligand (TRAIL) Apo-2L/TRAIL receptors.

scholarly journals The Prospects of tumor necrosis factor α inhibitors use in patients with COVID-19

2021 ◽  
Vol 15 (2) ◽  
pp. 89-93
Author(s):  
E. S. Aronova ◽  
B. S. Belov
Keyword(s):  
Clinical Trials ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Randomized Clinical Trials ◽  
Treatment Strategies ◽  
Current Data ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

The review highlights the problem of finding new effective treatment strategies for COVID-19. Tumor necrosis factor α (TNF-α) is considered as a therapeutic target. The theoretical basis for the successful use of TNF-α inhibitors (ITNFα) for the treatment of COVID-19 is presented, as well as data on existing practical developments, including ongoing clinical trials. Two drugs from the group of ITNFα – infliximab and adalimumab – are currently being considered as possible options. The safety issues of ITNFα treatment in patients with immunophaling rheumatic diseases and COVID-19 are discussed. The review also provides current data on vaccination against COVID-19, in particular on the vaccines currently available in Russia, which are at different stages of clinical trials. We conclude that randomized clinical trials of the effectiveness and safety of ITNF-α in patients with the new coronavirus infection are needed. Such trials will promote transition from theoretical speculations to real clinical practice.

scholarly journals Inflammatory Profile and Response to Anti-Tumor Necrosis Factor Therapy in Patients with Chronic Pulmonary Sarcoidosis

2011 ◽  
Vol 18 (6) ◽  
pp. 931-939 ◽  
Author(s):  
Matthew J. Loza ◽  
Carrie Brodmerkel ◽  
Roland M. Du Bois ◽  
Marc A. Judson ◽  
Ulrich Costabel ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Unknown Etiology ◽  
Infliximab Treatment ◽  
Tnf Α ◽  
Associated Proteins ◽  
Inflammatory Profile ◽  
Necrosis Factor

ABSTRACTSarcoidosis is an inflammatory, granulomatous disease of unknown etiology that most commonly afflicts the lungs. Despite aggressive immunosuppressive therapies, many sarcoidosis patients still chronically present significant symptoms. Infliximab, a therapeutic tumor necrosis factor alpha (TNF-α) monoclonal antibody (MAb), produced a small but significant improvement in forced vital capacity (FVC) in sarcoidosis patients in a double-blind, placebo-controlled, phase II clinical trial. In the current study, serum samples from this clinical trial were assessed to evaluate the underlying hypothesis that treatment with infliximab would reduce systemic inflammation associated with sarcoidosis, correlating with the extent of clinical response. A 92-analyte multiplex panel was used to assess the expression of serum proteins in 134 sarcoidosis patients compared with sera from 50 healthy controls. A strong systemic inflammatory profile was associated with sarcoidosis, with 29 analytes significantly elevated in sarcoidosis (false-discovery rate, <0.05 and >50% higher than controls). The associated analytes included chemokines, neutrophil-associated proteins, acute-phase proteins, and metabolism-associated proteins. This profile was evident despite patients receiving corticosteroids and immunosuppressive therapies. Following infliximab treatment, sarcoidosis patients expressing the highest levels of TNF-α, who had more severe disease, had the greatest improvement in FVC and reduction in serum levels of the inflammatory proteins MIP-1β and TNF-RII. This study supports the need for further exploration of anti-TNF therapy for chronic sarcoidosis patients, particularly for those expressing the highest serum levels of TNF-α.

scholarly journals TRAIL and FasL Functions in Cancer and Autoimmune Diseases: Towards an Increasing Complexity

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 639 ◽  
Author(s):  
Aurélie Rossin ◽  
Giorgia Miloro ◽  
Anne-Odile Hueber
Keyword(s):  
Tumor Necrosis Factor ◽  
Autoimmune Diseases ◽  
Tumor Necrosis ◽  
Fas Ligand ◽  
Current Knowledge ◽  
Receptor Gene ◽  
Critical Role ◽  
Effector Proteins ◽  
Immune Functions ◽  
Necrosis Factor

Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL/TNFSF10) and Fas Ligand (FasL/TNFSF6), two major cytokines of the TNF (Tumor Necrosis Factor) superfamily, exert their main functions from the immune system compartment. Mice model studies revealed that TRAIL and FasL-mediated signalling both control the homeostasis of the immune cells, mainly from the lymphoid lineage, and function on cytotoxic cells as effector proteins to eliminate the compromised cells. The first clues in the physiological functions of TRAIL arose from the analysis of TRAIL deficient mice, which, even though they are viable and fertile, are prone to cancer and autoimmune diseases development, revealing TRAIL as an important safeguard against autoimmunity and cancer. The naturally occurring gld (generalized lymphoproliferative disease) and lpr (lymphoproliferation) mutant mice develop lymphadenopathy and lupus-like autoimmune disease. The discovery that they are mutated in the fasl and the fas receptor gene, respectively, demonstrates the critical role of the FasL/Fas system in lymphocyte homeostasis and autoimmunity. This review summarizes the state of current knowledge regarding the key death and non-death immune functions that TRAIL and FasL play in the initiation and progression of cancer and autoimmune diseases.

scholarly journals The Tumor Necrosis Factor Superfamily of Cytokines in the Inflammatory Myopathies: Potential Targets for Therapy

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Boel De Paepe ◽  
Kim K. Creus ◽  
Jan L. De Bleecker
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Inflammatory Myopathies ◽  
Necrosis Factor Alpha ◽  
Tnf Superfamily ◽  
Sporadic Inclusion Body Myositis ◽  
Factor Alpha ◽  
Necrosis Factor

The idiopathic inflammatory myopathies (IM) represent a heterogeneous group of autoimmune diseases, of which dermatomyositis (DM), polymyositis (PM), and sporadic inclusion body myositis (IBM) are the most common. The crucial role played by tumor necrosis factor alpha (TNFα) in the IM has long been recognized. However, so far, 18 other members of the TNF superfamily have been characterized, and many of these have not yet received the attention they deserve. In this paper, we summarize current findings for all TNF cytokines in IM, pinpointing what we know already and where current knowledge fails. For each TNF family member, possibilities for treating inflammatory diseases in general and the IM in particular are explored.

scholarly journals Clinical Pharmacology Aspects in Patients Treated with TNF Inhibitors During SARS-Cov-2 Pandemic

2020 ◽  
Vol 11 (3) ◽  
pp. 393-394
Author(s):  
Francesco Ferrara ◽  
Priscilla Santilli ◽  
Vilma D'Aiuto ◽  
Antonio Vitiello
Keyword(s):  
Risk Factors ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Current Knowledge ◽  
Tnf Inhibitors ◽  
Global Pandemic ◽  
Increased Risk ◽  
Key Factor ◽  
Drug Treatments ◽  
Necrosis Factor

In this period of global pandemic caused by SARS-Cov-2, it is of paramount importance to recognize all risk factors that may increase the likelihood of infection. In addition to the risk factors known as pre-existing diseases and old age, risk factors could be drug treatments for chronic diseases, such as immunomodulating drugs that can alter immune defences and response to infectious agents. Antibodies that inhibit tumor necrosis factor (TNF) such as adalimumab infliximab etanercept and golimumab have been used for over 20 years in severe cases of autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease or ankylosing spondylitis. Due to their mechanism of action they reduce inflammation and can stop the progression of the disease by inhibiting a key factor of inflammation such as Tumor Necrosis Factor (TNF). In this article we want to examine the possible correlation between therapy with TNF inhibitors and the increased risk of SARS-CoV-2 infection, and the possible paradoxical therapeutic efficacy in patients with ongoing infection, especially in phase two and three. We express our opinion on this very complex and sensitive topic which is the subject of discussion among physicians and experts, based on current knowledge of the literature.

scholarly journals Elevated serum osteoprotegerin levels in women: friend or foe?

2015 ◽  
Vol 61 (6) ◽  
pp. 524-529 ◽  
Author(s):  
Gisela Rodrigues da Silva Sasso ◽  
Rinaldo Florencio-Silva ◽  
Ricardo Santos Simões ◽  
Maria Cândida Pinheiro Baracat ◽  
José Maria Soares Júnior ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Tumor Necrosis Factor ◽  
Bone Tissue ◽  
Tumor Necrosis ◽  
Elevated Serum ◽  
Therapeutic Interventions ◽  
Nuclear Factor ◽  
Mesh Terms ◽  
Nuclear Factor Kb ◽  
Necrosis Factor

SUMMARY Introduction: osteoprotegerin has emerged as a new candidate for the treatment of osteoporosis. However, high levels of osteoprotegerin have been linked to vascular calcification, an independent and well-defined risk factor for cardiovascular disease (CVD) and mortality. Thus, the action of osteoprotegerin in these situations has been questioned. Objective: to evaluate the effect of osteoprotegerin (OPG) on the human body, especially in bone tissue and in vascular diseases. Methods: the scientific databases consulted were PubMed-Medline and Cochrane, using keywords (MeSH terms) grouped into the following syntaxes: (Osteoprotegerin OR Osteoclastogenesis Inhibitory Factor OR Receptors, Tumor Necrosis Factor, Member 11b OR Tumor Necrosis Factor Receptor Superfamily, Member 11b OR FDCR-1 Protein OR FDCR 1 Protein OR OCIF Protein OR Follicular Dendritic Cell-Derived Receptor-1) AND (Bones AND Bone OR Bones AND Bone Tissue OR Bones OR Bone Tissue OR Cardiovascular Diseases). Results: Osteoprotegerin is present in various organs and binds to two ligands: nuclear factor kB (RANKL) related to the differentiation of osteoclasts, and tumor necrosis factor related to the apoptosis-inducing ligand (TRAIL). OPG inhibits the regulation effects of nuclear factor kB on inflammation and on the skeletal and vascular systems, preventing the apoptosis induced by TRAIL, being related to the preservation of bone tissue. Conclusion: a deeper knowledge of the mechanisms involved in the association between OPG serum levels, bone integrity and cardiovascular disease can provide important data for future therapeutic interventions.

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