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  3. CMS
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  5. How Does Doi.org Make Money
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We began analyzing https://www.nature.com/articles/s41419-019-1370-2, but it redirected us to https://www.nature.com/articles/s41419-019-1370-2. The analysis below is for the second page.

Title[redir]:
Cell death pathways in pathogenic trypanosomatids: lessons of (over)kill | Cell Death & Disease
Description:
Especially in tropical and developing countries, the clinically relevant protozoa Trypanosoma cruzi (Chagas disease), Trypanosoma brucei (sleeping sickness) and Leishmania species (leishmaniasis) stand out and infect millions of people worldwide leading to critical social-economic implications. Low-income populations are mainly affected by these three illnesses that are neglected by the pharmaceutical industry. Current anti-trypanosomatid drugs present variable efficacy with remarkable side effects that almost lead to treatment discontinuation, justifying a continuous search for alternative compounds that interfere with essential and specific parasite pathways. In this scenario, the triggering of trypanosomatid cell death machinery emerges as a promising approach, although the exact mechanisms involved in unicellular eukaryotes are still unclear as well as the controversial biological importance of programmed cell death (PCD). In this review, the mechanisms of autophagy, apoptosis-like cell death and necrosis found in pathogenic trypanosomatids are discussed, as well as their roles in successful infection. Based on the published genomic and proteomic maps, the panel of trypanosomatid cell death molecules was constructed under different experimental conditions. The lack of PCD molecular regulators and executioners in these parasites up to now has led to cell death being classified as an unregulated process or incidental necrosis, despite all morphological evidence published. In this context, the participation of metacaspases in PCD was also not described, and these proteases play a crucial role in proliferation and differentiation processes. On the other hand, autophagic phenotype has been described in trypanosomatids under a great variety of stress conditions (drugs, starvation, among others) suggesting that this process is involved in the turnover of damaged structures in the protozoa and is not a cell death pathway. Death mechanisms of pathogenic trypanosomatids may be involved in pathogenesis, and the identification of parasite-specific regulators could represent a rational and attractive alternative target for drug development for these neglected diseases.

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 8,815,392 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We're unsure if the website is profiting.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

pubmed, article, google, scholar, death, cell, cas, autophagy, trypanosomatids, central, autophagic, atg, cruzi, trypanosoma, apoptosis, parasite, programmed, disease, leishmania, brucei, pcd, differentiation, pathway, nature, protozoa, necrosis, molecular, parasites, mitochondrial, pathogenic, drugs, molecules, role, apoptotic, apoptosislike, mechanisms, pathways, chagas, process, drug, stress, forms, membrane, activity, parasitol, leishmaniasis, treatment, metacaspases, dna, including,

Topics {✒️}

nature portfolio privacy policy drug discovery research advertising molecular tools social media research priorities cysteine-dependent aspartate-directed proteases enzymatic kits nature 390 nature 407 nature 403 nature 406 nature reprints bcl-xl anti-apoptotic proteins article menna-barreto india fadd-homologous ice/ced-3 innovative semi-synthetic thiosemicarbazone l-arginine-dependent suppression open questions lysosomal hydrolase-dependent degradation papes/fundação oswaldo cruz author information authors previous data showed int/neglected_diseases/2010report/en/ open promising anti-protozoan peptide central nervous system death-inducing signaling complex int/neglected_diseases/diseases/en/ large-scale proteomic studies permissions ros-dependent cell death author correspondence original author pro-apoptotic nuclease activity high ros content metacaspase-independent death pathway critical social-economic implications complement system-based therapeutics morphological evidence published plasma membrane disruption molecules trigger/suppress autophagy autophagy-independent cell death personal data human african trypanosomiasis menna-barreto menna-barreto

Questions {❓}

  • Are apoptotic-like and autophagic pathways good drug targets in trypanosomatids?
  • Are protozoan metacaspases potential parasite killers?
  • Autophagosomes: biogenesis from scratch?
  • Autophagy in cell death: an innocent convict?
  • Autophagy: dual roles in life and death?
  • Blocking autophagy to prevent parasite differentiation: a possible new strategy for fighting parasitic infections?
  • Cell death in Leishmania induced by stress and differentiation: programmed cell death or necrosis?
  • Cell death in parasitic protozoa: regulated or incidental?
  • Kinetoplastida: model organisms for simple autophagic pathways?
  • Necrosis: a specific form of programmed cell death?
  • Programmed cell death in trypanosomatids: a way to maximize their biological fitness?
  • Stairway to heaven or hell?
  • What are the molecular mechanisms involved in protozoan autophagy?
  • What is the real biological relevance of programmed cell death in protozoa?
  • Which molecules participate in apoptotic-like activation/regulation in trypanosomatids?
  • Which molecules trigger/suppress autophagy in these protozoa?

Schema {🗺️}

WebPage:
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         headline:Cell death pathways in pathogenic trypanosomatids: lessons of (over)kill
         description:Especially in tropical and developing countries, the clinically relevant protozoa Trypanosoma cruzi (Chagas disease), Trypanosoma brucei (sleeping sickness) and Leishmania species (leishmaniasis) stand out and infect millions of people worldwide leading to critical social-economic implications. Low-income populations are mainly affected by these three illnesses that are neglected by the pharmaceutical industry. Current anti-trypanosomatid drugs present variable efficacy with remarkable side effects that almost lead to treatment discontinuation, justifying a continuous search for alternative compounds that interfere with essential and specific parasite pathways. In this scenario, the triggering of trypanosomatid cell death machinery emerges as a promising approach, although the exact mechanisms involved in unicellular eukaryotes are still unclear as well as the controversial biological importance of programmed cell death (PCD). In this review, the mechanisms of autophagy, apoptosis-like cell death and necrosis found in pathogenic trypanosomatids are discussed, as well as their roles in successful infection. Based on the published genomic and proteomic maps, the panel of trypanosomatid cell death molecules was constructed under different experimental conditions. The lack of PCD molecular regulators and executioners in these parasites up to now has led to cell death being classified as an unregulated process or incidental necrosis, despite all morphological evidence published. In this context, the participation of metacaspases in PCD was also not described, and these proteases play a crucial role in proliferation and differentiation processes. On the other hand, autophagic phenotype has been described in trypanosomatids under a great variety of stress conditions (drugs, starvation, among others) suggesting that this process is involved in the turnover of damaged structures in the protozoa and is not a cell death pathway. Death mechanisms of pathogenic trypanosomatids may be involved in pathogenesis, and the identification of parasite-specific regulators could represent a rational and attractive alternative target for drug development for these neglected diseases.
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      headline:Cell death pathways in pathogenic trypanosomatids: lessons of (over)kill
      description:Especially in tropical and developing countries, the clinically relevant protozoa Trypanosoma cruzi (Chagas disease), Trypanosoma brucei (sleeping sickness) and Leishmania species (leishmaniasis) stand out and infect millions of people worldwide leading to critical social-economic implications. Low-income populations are mainly affected by these three illnesses that are neglected by the pharmaceutical industry. Current anti-trypanosomatid drugs present variable efficacy with remarkable side effects that almost lead to treatment discontinuation, justifying a continuous search for alternative compounds that interfere with essential and specific parasite pathways. In this scenario, the triggering of trypanosomatid cell death machinery emerges as a promising approach, although the exact mechanisms involved in unicellular eukaryotes are still unclear as well as the controversial biological importance of programmed cell death (PCD). In this review, the mechanisms of autophagy, apoptosis-like cell death and necrosis found in pathogenic trypanosomatids are discussed, as well as their roles in successful infection. Based on the published genomic and proteomic maps, the panel of trypanosomatid cell death molecules was constructed under different experimental conditions. The lack of PCD molecular regulators and executioners in these parasites up to now has led to cell death being classified as an unregulated process or incidental necrosis, despite all morphological evidence published. In this context, the participation of metacaspases in PCD was also not described, and these proteases play a crucial role in proliferation and differentiation processes. On the other hand, autophagic phenotype has been described in trypanosomatids under a great variety of stress conditions (drugs, starvation, among others) suggesting that this process is involved in the turnover of damaged structures in the protozoa and is not a cell death pathway. Death mechanisms of pathogenic trypanosomatids may be involved in pathogenesis, and the identification of parasite-specific regulators could represent a rational and attractive alternative target for drug development for these neglected diseases.
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Social Networks {👍}(1)

External Links {🔗}(698)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
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Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
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Name Servers:

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CDN Services {📦}

  • Crossref

5.69s.