<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1870-7203</journal-id>
<journal-title><![CDATA[Acta médica Grupo Ángeles]]></journal-title>
<abbrev-journal-title><![CDATA[Acta méd. Grupo Ángeles]]></abbrev-journal-title>
<issn>1870-7203</issn>
<publisher>
<publisher-name><![CDATA[Grupo Ángeles, Servicios de Salud]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1870-72032025000100041</article-id>
<article-id pub-id-type="doi">10.35366/119347</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Caminos fisiopatológicos y blancos terapéuticos actuales para nefropatía diabética en diabetes tipo 1 y 2]]></article-title>
<article-title xml:lang="en"><![CDATA[Current physiopathological pathways and therapeutic targets for diabetic nephropathy in type 1 and 2 diabetes]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Díaz Greene]]></surname>
<given-names><![CDATA[Enrique Juan]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sánchez Arreguín]]></surname>
<given-names><![CDATA[Roxana]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bautista Martínez]]></surname>
<given-names><![CDATA[Brenda]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital Angeles Pedregal  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Hospital Angeles Pedregal Servicio Social ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2025</year>
</pub-date>
<volume>23</volume>
<numero>1</numero>
<fpage>41</fpage>
<lpage>46</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1870-72032025000100041&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1870-72032025000100041&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1870-72032025000100041&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: El riñón es un órgano con gran importancia funcional debido a que regula los niveles de líquidos corporales y con ello la presión arterial, ayuda en el mantenimiento óseo y es fundamental en la hematopoyesis. En pacientes con diabetes tipo 1 y 2, una de las principales complicaciones es la nefropatía pues esta patología induce cambios fisiopatológicos que afectan el adecuado funcionamiento del riñón. El mecanismo de la nefropatía diabética consiste en la alteración de la homeostasis en la hemodinámica renal, ocasionando hipertensión glomerular, isquemia e hipoxia, un incremento en el estrés oxidativo y regulación al alza del sistema renina-aldosterona, lo que ocasiona manifestaciones clínicas como albuminuria, disminución en la tasa de filtrado glomerular y enfermedad renal. Actualmente existen terapias que se basan en el control de los cambios en la hemodinámica renal, en el sistema renina-aldosterona, hipertensión glomerular, isquemia e hipoxia, tales como el control de la glucosa y presión arterial, inhibidores del sistema renina-angiotensina, antagonistas del receptor de mineralocorticoides e inhibidores del cotransportador sodio-glucosa. Actualmente se han investigado nuevos blancos terapéuticos con la finalidad de intervenir en la progresión de los cambios fisiopatológicos de la nefropatía diabética y los mecanismos que la originan.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: The kidney is an organ with great functional importance; it regulates body fluid levels and blood pressure, helps in bone maintenance, and is essential in hematopoiesis. In patients with type 1 and 2 diabetes, one of the main complications is nephropathy since this pathology induces pathophysiological changes that affect the proper functioning of the kidney. The mechanism of diabetic nephropathy consists of alterations in homeostasis in renal hemodynamics, causing glomerular hypertension, ischemia, and hypoxia, an increase in oxidative stress, and upregulation of the renin-aldosterone system, which causes clinical manifestations such as albuminuria, decreased glomerular filtration rate and kidney disease. Currently, some therapies are based on the control of changes in renal hemodynamics, in the renin-aldosterone system, glomerular hypertension, ischemia, and hypoxia, such as control of glucose and blood pressure, inhibitors of the renin-angiotensin system, mineralocorticoid receptor antagonists and sodium-glucose cotransporter inhibitors. Currently, new therapeutic targets have been investigated to intervene in the progression of the pathophysiological changes of diabetic nephropathy and the mechanisms that give origin to it.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[nefropatía]]></kwd>
<kwd lng="es"><![CDATA[hipoxia]]></kwd>
<kwd lng="es"><![CDATA[estrés oxidativo]]></kwd>
<kwd lng="es"><![CDATA[proteinuria]]></kwd>
<kwd lng="es"><![CDATA[blancos terapéuticos]]></kwd>
<kwd lng="en"><![CDATA[nephropathy]]></kwd>
<kwd lng="en"><![CDATA[hypoxia]]></kwd>
<kwd lng="en"><![CDATA[oxidative stress]]></kwd>
<kwd lng="en"><![CDATA[proteinuria]]></kwd>
<kwd lng="en"><![CDATA[therapeutic targets]]></kwd>
</kwd-group>
</article-meta>
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<page-range>1598-601</page-range></nlm-citation>
</ref>
</ref-list>
</back>
</article>
