Jump to content
  • mission_statement.pngrrdiLogo384x64.jpg.3cd1bd79f5d066075bdd9

    Mission Statement

    The Rosacea Research & Development Institute [RRDi] is the first non-profit organization made by rosaceans for rosacea sufferers that will collect donations for rosacea research to be performed by physicians and biomedical research scientists and includes these specific goals:

    Goal # 1: To be the first non profit organization for rosacea patient advocacy and to find the cure for rosacea. 

    Goal # 2: To have a majority of rosaceans the right to vote who sits on the board of directors. This is in stark contrast to other rosacea non profit organizations comprised of non rosacea sufferers who are usually businessmen or dermatologists with a vested interest in treating rosacea. 

    Goal # 3: To make this the first rosacea specific non profit organization to utilize most of the donations for research and treatment development. This is in stark contrast to non profit organizations that spend 50% to 60% of their donations on paying their staff, board of directors, conventions for professional members or to pay private contractors for services.

    Goal # 4: To allow rosacea sufferers to guide where and how the money is spent on rosacea research and be the first non profit organization to allow rosaceans to be members of the corporation. Until June 7, 2004, the date of incorporation, there had been no other non profit organization that allowed input from rosacea sufferers.

    Goal # 5: To attain a level such that the RRDi can directly impact medical articles published on the subject, information disseminated to physicians and rosacea sufferers and apply positive pressure on the medical community.

    Goal #6: Continue to publish the Journal of the RRDi and fund all authors who contribute an article.

    Goal #7: To allow volunteer members to have a platform to voice their concerns about rosacea and to contribute information about rosacea. Our goal is 10K members. 

    For more information on how and why this non profit organization for rosacea was formed click here.

    Our Charter can be read by clicking here.

     



  • Member Statistics

    • Total Members
      1,672
    • Most Online
      499

    Newest Member
    sebdermhelp
    Joined
  • image.png.9c7b476f653b05bf0b4220389b0df3

  • Posts

    • Front Pharmacol. 2023 Mar 1;14:1092473. doi: 10.3389/fphar.2023.1092473. eCollection 2023. ABSTRACT Background: Rosacea is a common facial skin inflammatory disease featured by hyperactivation of mTORC1 signaling in the epidermis. Due to unclear pathogenesis, the effective treatment options for rosacea remain limited. Methods: Weighted gene co-expression network analysis (WGCNA) analyzed the relationship between epidermis autophagy and mTOR pathways in rosacea, and further demonstrated it through immunofluorescence and qPCR analysis. A potential therapeutic agent for rosacea was predicted based on the key genes of the WGCNA module. In vivo and in vitro experiments were conducted to verify its therapeutic role. Drug-target prediction (TargetNet, Swiss, and Tcmsp) and molecular docking offered potential pharmacological targets. Results: WGCNA showed that epidermis autophagy was related to the activation of mTOR pathways in rosacea. Next, autophagy was downregulated in the epidermis of rosacea, which was regulated by mTOR. In addition, the in vivo experiment demonstrated that autophagy induction could be an effective treatment strategy for rosacea. Subsequently, based on the key genes of the WGCNA module, epigallocatechin-3-gallate (EGCG) was predicted as a potential therapeutic agent for rosacea. Furthermore, the therapeutic role of EGCG on rosacea was confirmed in vivo and in vitro. Finally, drug-target prediction and molecular docking revealed that AKT1/MAPK1/MMP9 could be the pharmacological targets of EGCG in rosacea. Conclusion: Collectively, our findings revealed the vital role of autophagy in rosacea and identified that EGCG, as a therapeutic agent for rosacea, attenuated rosacea-like inflammation via inducing autophagy in keratinocytes. PMID:36937834 | PMC:PMC10014537 | DOI:10.3389/fphar.2023.1092473 {url} = URL to article
×
×
  • Create New...

Important Information

Terms of Use