Erick Martínez Herrera

Dr. Erick Martínez Herrera

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Díaz Mirón, Ciudad de México 11340, Mexico
orcid

Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
2 September 2020 in Antibiotics
Verified
Journal Article
Open access
PDF file
MFMaría Guadalupe Frías-De-León
María Guadalupe Frías-De-León
RHRigoberto Hernandez-Castro
Rigoberto Hernandez-Castro
TVTania Mayela Vite-Garín
Tania Mayela Vite-Garín
RARoberto Arenas
Roberto Arenas
ABAlexandro Bonifaz
Alexandro Bonifaz
Erick Martínez HerreraErick Martínez Herrera
Erick Martínez Herrera
Since Candida auris integrates strains resistant to multiple antifungals, research has been conducted focused on knowing which molecular mechanisms are involved. This review aims to summarize the results obtained in some of these studies. A search was carried out by consulting websites and online databases. The analysis indicates that most C. auris strains show higher resistance to fluconazole, followed by amphotericin B, and less resistance to 5-fluorocytosine and caspofungin. In C. auris, antifungal resistance to amphotericin B has been linked to an overexpression of several mutated ERG genes that lead to reduced ergosterol levels; fluconazole resistance is mostly explained by mutations identified in the ERG11 gene, as well as a higher number of copies of this gene and the overexpression of efflux pumps. For 5-fluorocytosine, it is hypothesized that the resistance is due to mutations in the FCY2, FCY1, and FUR1 genes. Resistance to caspofungin has been associated with a mutation in the FKS1 gene. Finally, resistance to each antifungal is closely related to the type of clade to which the strain belongs.

25 September 2020 in Journal of the European Academy of Dermatology and Venereology
Verified
Journal Article
Closed access
PDF file
Carmen Rodriguez-CerdeiraCarmen Rodriguez-Cerdeira
Carmen Rodriguez-Cerdeira
Erick Martínez HerreraErick Martínez Herrera
Erick Martínez Herrera
Jacek C. SzepietowskiJacek C. Szepietowski
Jacek C. Szepietowski
Rodolfo Pinto-AlmazánRodolfo Pinto-Almazán
Rodolfo Pinto-Almazán
MFM.G. Frías‐De‐León
M.G. Frías‐De‐León
DSDitte Marie Lindhardt Saunte
Ditte Marie Lindhardt Saunte

22 September 2021 in Pharmaceutics
Verified
Journal Article
Open access
PDF file
MFMaría Guadalupe Frías-De-León
María Guadalupe Frías-De-León
RHRigoberto Hernandez-Castro
Rigoberto Hernandez-Castro
ECEsther Conde-Cuevas
Esther Conde-Cuevas
ICItzel Hayde García Coronel
Itzel Hayde García Coronel
VVVíctor Alfonso Vázquez-Aceituno
Víctor Alfonso Vázquez-Aceituno
Erick Martínez HerreraErick Martínez Herrera
Erick Martínez Herrera
In recent years, a progressive increase in the incidence of invasive fungal infections (IFIs) caused by Candida glabrata has been observed. The objective of this literature review was to study the epidemiology, drug resistance, and virulence factors associated with the C. glabrata complex. For this purpose, a systematic review (January 2001–February 2021) was conducted on the PubMed, Scielo, and Cochrane search engines with the following terms: “C. glabrata complex (C. glabrata sensu stricto, C. nivariensis, C. bracarensis)” associated with “pathogenicity” or “epidemiology” or “antibiotics resistance” or “virulence factors” with language restrictions of English and Spanish. One hundred and ninety-nine articles were found during the search. Various mechanisms of drug resistance to azoles, polyenes, and echinocandins were found for the C. glabrata complex, depending on the geographical region. Among the mechanisms found are the overexpression of drug transporters, gene mutations that alter thermotolerance, the generation of hypervirulence due to increased adhesion factors, and modifications in vital enzymes that produce cell wall proteins that prevent the activity of drugs designed for its inhibition. In addition, it was observed that the C. glabrata complex has virulence factors such as the production of proteases, phospholipases, and hemolysins, and the formation of biofilms that allows the complex to evade the host immune response and generate fungal resistance. Because of this, the C. glabrata complex possesses a perfect pathogenetic combination for the invasion of the immunocompromised host.

10 October 2016 in BMC Infectious Diseases
Verified
Journal Article
Open access
PDF file
MRMaría del Rocío Reyes-Montes
María del Rocío Reyes-Montes
MPMaría Ameyali Pérez-Huitrón
María Ameyali Pérez-Huitrón
JOJorge Luis Ocaña-Monroy
Jorge Luis Ocaña-Monroy
MFMaría Guadalupe Frías-De-León
María Guadalupe Frías-De-León
Erick Martínez HerreraErick Martínez Herrera
Erick Martínez Herrera
Esperanza Duarte-EscalanteEsperanza Duarte-Escalante
Esperanza Duarte-Escalante
Coccidioidomycosis, a potentially fatal fungal infection, is considered an emergent mycotic disease because of the increased incidence of fungal infections registered over recent years. Infection occurs through the inhalation of arthroconidia from two main species of Coccidioides: Coccidioides immitis and C. posadasii, which are both endemic to arid and semi-arid regions of North America. Coccidioides species not only infect humans but can also infect other mammals (land, aquatic, wild or domestic), reptiles and birds. To obtain information regarding the habitat of Coccidioides spp. and the animals infected by this fungus and to identify the role that infected animals play as reservoirs and disseminators of this fungus in nature. A literature review was conducted to identify the habitat of Coccidioides spp. and the infected non-human animal species targeted by this fungus. This review allows us to suggest that Coccidioides spp. may be classified as halotolerant organisms; nevertheless, to perpetuate their life cycle, these organisms depend on different animal species (reservoirs) that serve as a link with the environment, by acting as disseminators of the fungi in nature.

28 May 2019 in Mediators of Inflammation
Verified
Journal Article
Open access
PDF file
Carmen Rodriguez-CerdeiraCarmen Rodriguez-Cerdeira
Carmen Rodriguez-Cerdeira
MCMónica Cordeiro-Rodríguez
Mónica Cordeiro-Rodríguez
MGMiguel Carnero Gregorio
Miguel Carnero Gregorio
ALAdriana López-Barcenas
Adriana López-Barcenas
Erick Martínez HerreraErick Martínez Herrera
Erick Martínez Herrera
JGJosé Luís González-Cespón
José Luís González-Cespón
Psoriasis is a common chronic inflammatory multisystemic disease with a complex pathogenesis consisting of genetic, immunological, and environmental components. It is associated with a number of comorbidities, including diabetes, metabolic syndrome, obesity, and myocardial infarction. In addition, the severity of psoriasis seems to be related to the severity of obesity. Patients with higher levels of obesity show poorer response to systemic treatments of psoriasis. Several studies have demonstrated that white adipose tissue is a crucial site of the formation of proinflammatory adipokines such as leptin, adiponectin, and resistin and classical cytokines such as interleukin- (IL-) 6 and tumour necrosis factor-α. In psoriasis, due to the proliferation of Th1, Th17, and Th22 cells, IL-22, among others, is produced in addition to the abovementioned cytokines. With respect to leptin and resistin, both of these adipokines are present in high levels in obese persons with psoriasis. Further, the plasma levels of leptin and resistin are related to the severity of psoriasis. These results strongly suggest that obesity, through proinflammatory pathways, is a predisposing factor to the development of psoriasis and that obesity aggravates existing psoriasis. Different inflammatory biomarkers link psoriasis and obesity. In this paper, the most important ones are described.

30 May 2022 in Journal of Fungi
Verified
Journal Article
Open access
PDF file
RHRigoberto Hernandez-Castro
Rigoberto Hernandez-Castro
Rodolfo Pinto-AlmazánRodolfo Pinto-Almazán
Rodolfo Pinto-Almazán
RARoberto Arenas
Roberto Arenas
CSCarlos Sánchez
Carlos Sánchez
VEVíctor Manuel Espinosa-Hernández
Víctor Manuel Espinosa-Hernández
Carmen Rodriguez-CerdeiraCarmen Rodriguez-Cerdeira
Carmen Rodriguez-Cerdeira
Background: Sporotrichosis is a fungal infection caused by species of the Sporothrix genus. Presently, the prevalence of sporotrichosis in the Americas is unknown, so this study aims to analyze the cases reported in the past 10 years. Methods: An advanced search was conducted from 2012 to 2022 in English and Spanish in PUBMED, SciELO, and Cochrane, with the terms: “sporotrichosis”, “lymphocutaneous sporotrichosis”, “fixed sporotrichosis”, “mycosis”, “Sporothrix spp.”, “Sporothrix complex”, “S. schenckii sensu stricto”, “S. schenckii sensu lato”, “S. globose”, “S. brasiliensis”, “S. luriei”. Sporotrichosis is a fungal infection caused by species of the Sporothrix genus associated with “pathogenicity” or “epidemiology”. Results: A total of 124 articles were found in the Americas, corresponding to 12,568 patients. Of these, 87.38% of cases were reported in South America, 11.62% in North America, and 1.00% in Central America and the Caribbean. Brazil, Peru, and Mexico had the highest number of cases. The most prevalent etiological agents were S. schenckii complex/Sporothrix spp. (52.91%), S. schenckii (42.38%), others (4.68%), and Not Determined (ND) (0.03%). The most frequent form of the disease was lymphocutaneous infection; however, the infection type was not determined in 5639 cases. Among the diagnostic methods, culture was the most used. Conclusions: There is a high occurrence of cases reported in the literature. South America is the region with the highest number of reports because of its environment (climate, inhalation of spores, etc.), zoonotic transmission (scratches and sneezes from contaminated animals), and possible traumatic inoculation due to outdoor activities (agriculture, gardening, and related occupations). Molecular diagnosis has not been sufficiently developed due to its high cost.