Trends in Molecular Medicine (TRENDS MOL MED )

Publisher: Elsevier

Description

Trends in Molecular Medicine's objective is to facilitate communication between groups of highly trained professionals with distinct backgrounds and skills, whose common goals are to understand and explain the molecular basis of disease with a view to new clinical practice. Trends in Molecular Medicine is a resource for students and professionals alike, who have information needs that transcend the traditional clinical or scientific categorisation. Trends in Molecular Medicine includes review articles on the genetic basis of disease, but 'molecular' does not only mean DNA. The diagnostic role of genetic processes is clear, but major benefits in health and disease are also provided by other molecules: enzymes, antibiotics, hormones, metals, carbohydrates, lipids, vitamins, synthetic organic and inorganic polymers. Such benefits are discussed and evaluated by Trends in Molecular Medicine. Furthermore 'Medicine' involves a vital societal element; molecular intervention raises controversial ethical, legal and financial issues. All these issues are addressed in Trends in Molecular Medicine in a style that builds on 25 years' experience of publishing the Trends Journals.

  • Impact factor
    9.57
    Show impact factor history
     
    Impact factor
  • 5-year impact
    10.14
  • Cited half-life
    5.40
  • Immediacy index
    1.49
  • Eigenfactor
    0.02
  • Article influence
    3.84
  • Website
    Trends in Molecular Medicine website
  • Other titles
    Trends in molecular medicine (Online)
  • ISSN
    1471-4914
  • OCLC
    45949985
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
    • Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PMC after 12 months
    • Authors who are required to deposit in subject repositories may also use Sponsorship Option
    • Pre-print can not be deposited for The Lancet
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Over the past two decades complementary and alternative medicine treatments relying on dubious science have been embraced by medical academia. Despite low to nonexistent prior probability that testing these treatments in randomized clinical trials (RCTs) will be successful, RCTs of these modalities have proliferated, consistent with the principles of evidence-based medicine, which underemphasize prior plausibility rooted in science. We examine this phenomenon and argue that what is needed is science-based medicine rather than evidence-based medicine.
    Trends in Molecular Medicine 08/2014;
  • Trends in Molecular Medicine 05/2014;
  • Trends in Molecular Medicine 05/2014;
  • Trends in Molecular Medicine 03/2013;
  • Source
    Trends in Molecular Medicine 01/2012;
  • Article: letter 13
    Trends in Molecular Medicine 01/2010;
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    ABSTRACT: Colorectal cancer (CRC) is characterized by the partial suppression of apoptosis, which in turn gives tumours a selective advantage for survival and can cause current chemotherapy approaches to be ineffective. Recent progress in understanding the mechanisms of apoptosis in colorectal carcinogenesis has provided potential new targets for therapy. Here, we review recent studies of the regulation of apoptosis and its role in CRC initiation and progression, and we discuss the relationship between chemoresistance and the suppression of apoptosis. Recent progress in targeting apoptotic pathways and their regulators provide strategies for the exploration of novel therapies for CRC.
    Trends in Molecular Medicine 05/2009; 15(5):225-33.
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    ABSTRACT: Osteoblasts are key components of the bone multicellular unit and have a seminal role in bone remodeling, which is an essential function for the maintenance of the structural integrity and metabolic capacity of the skeleton. The coordinated function of skeletal cells is regulated by several hormones, growth factors and mechanical cues that act via interconnected signaling networks, resulting in the activation of specific transcription factors and, in turn, their target genes. Bone cells are responsive to mechanical stimuli and this is of pivotal importance in developing biomechanical strategies for the treatment of osteodegenerative diseases. Here, we review the molecular pathways and players activated by mechanical stimulation during osteoblastic growth, differentiation and activity in health, and consider the role of mechanostimulatory approaches in treating various bone pathophysiologies.
    Trends in Molecular Medicine 05/2009; 15(5):208-16.
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    ABSTRACT: Aging and degenerative diseases are associated with increased levels of reactive oxygen species (ROS). ROS are mostly produced in mitochondria, and their levels increase with higher mitochondrial membrane potential. Cellular respiratory control is based on inhibition of respiration by high membrane potentials. However, we have described a second mechanism of respiratory control based on allosteric inhibition of cytochrome c oxidase (CcO), the terminal enzyme of the respiratory chain, at high ATP:ADP ratios. The mechanism is independent of membrane potential. We have proposed that feedback inhibition of CcO by ATP keeps the membrane potential and ROS production at low levels. Various forms of stress switch off allosteric ATP-inhibition via reversible dephosphorylation of CcO, resulting in increased membrane potential and cellular ROS levels. This mechanism is proposed to represent a missing molecular link between stress and degenerative diseases.
    Trends in Molecular Medicine 05/2009; 15(4):139-47.
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    ABSTRACT: Whole-genome association studies (WGASs) have identified single-nucleotide polymorphisms (SNPs) associated with sporadic amyotrophic lateral sclerosis (sALS). However, WGASs have so far produced results that are not consistent with those obtained from monogenic association studies focused on genes found to be relevant to ALS in functional biological studies. We propose that such inconsistencies might be at least partially alleviated by using approaches that integrate weakly associated SNPs. Several independent studies have detected abnormal reverse transcriptase (RT) activity in sALS patients, suggesting the involvement of retroelements in ALS pathogenesis. Here, we discuss the functions of genes with SNPs or mutations in sALS and consider whether these might implicate the involvement of a putative retroelement associated with sALS pathogenesis. New experimental models for studying retroviral activation and the effects of xenobiotic agents in ALS will be needed to further investigate a potential role of retroelements in the etiology of sALS.
    Trends in Molecular Medicine 05/2009; 15(4):148-58.
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    ABSTRACT: Autophagy is involved in cellular protein and organelle degradation, which is mediated by the lysosomal pathway. Autophagocytosis has a key role in cellular housekeeping by removing damaged organelles. During aging, the efficiency of autophagic degradation declines and intracellular waste products accumulate. In Caenorhabditis elegans, there is clear evidence that lifespan is linked to the capacity to regulate autophagy. Recent studies have revealed that the same signaling factors regulate both aging and autophagocytosis, thus highlighting the role of autophagy in the regulation of aging and age-related degenerative diseases. Here, we examine in detail the interactions of the signaling network involving longevity factors SIRT1, mTOR, FoxO3, NF-kappaB and p53 in the regulation of autophagy. We discuss the possibility that these well-known stress resistance and longevity factors regulate the aging process via autophagy.
    Trends in Molecular Medicine 05/2009; 15(5):217-24.
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    ABSTRACT: Differentiation of naïve T cells leads to the generation of T-cell subsets, each possessing distinct cytokine expression profiles for serving different immune functions. Through the activation of separate signaling pathways, this process results in both differentiated helper T (Th) cells, termed Th1, Th2 and Th17, and induced regulatory T cells, which suppress Th cells. These different cells are important for combating infectious diseases and cancers; however, when aberrant, they can be responsible for chronic inflammatory diseases. One such disease is inflammatory bowel disease (IBD), in which each T-cell subset can have a role in disease. New studies highlight the importance of the recently identified Th17 subset in IBD. Therapeutics targeting these aberrant Th responses are already under development and hold promise for treating IBD and other chronic inflammatory diseases.
    Trends in Molecular Medicine 05/2009; 15(5):199-207.
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    ABSTRACT: Recent studies have shown that male reproductive function is modulated via the mitogen-activated protein kinase (MAPK) cascade. The MAPK cascade is involved in numerous male reproductive processes, including spermatogenesis, sperm maturation and activation, capacitation and acrosome reaction, before fertilization of the oocyte. In this review, we discuss the latest findings in this rapidly developing field regarding the role of MAPK in male reproduction in animal models and in human spermatozoa in vitro. This research will facilitate the design of future studies in humans, although much work is needed before this information can be used to manage male infertility and environmental toxicant-induced testicular injury in men, such as blood-testis-barrier disruption.
    Trends in Molecular Medicine 05/2009; 15(4):159-68.
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    ABSTRACT: Uniparental disomy (UPD) results when both copies of a chromosome pair originate from one parent. In humans, this might result in developmental disease or cancer due to either the production of homozygosity (caused by mutated or methylated genes or by microRNA sequences) or an aberrant pattern of imprinting. Constitutional UPD is associated with meiotic errors, resulting in developmental diseases, whereas acquired UPD probably occurs as a result of a mitotic error in somatic cells, which can be an important step in cancer development and progression. This review summarizes the mechanisms underlying UPD and their emerging association with cancer.
    Trends in Molecular Medicine 03/2009; 15(3):120-8.

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