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id="primary"> <main class="site-main" id="main"> <article id="post-79" class="post-79 post type-post status-publish format-standard has-post-thumbnail hentry category-diabetic-nephropathy tag-biomarkers tag-diabetic-nephropathy tag-fibrosis tag-glomerulosclerosis tag-inflammation tag-jak-stat tag-novel-therapies tag-oxidative-stress tag-renin-angiotensin-system tag-soce tag-store-operated-calcium-entry tag-tgf- tag-therapeutic-targets" itemtype="https://schema.org/CreativeWork" itemscope> <div class="inside-article"> <div class="featured-image page-header-image-single "> <img width="1200" height="628" src="https://renaldisorders.com/archive/wp-content/uploads/2024/11/banner-39-min-scaled-e1730804794905.jpg" class="attachment-full size-full" alt="" itemprop="image" decoding="async" fetchpriority="high" /> </div> <header class="entry-header"> <h1 class="entry-title" itemprop="headline">Advances in Therapeutic Targets for Diabetic Nephropathy</h1> <div class="entry-meta"> <span class="posted-on"><time class="entry-date published" datetime="2024-11-05T16:36:50+05:30" itemprop="datePublished">November 5, 2024</time></span> <span class="byline">by <span class="author vcard" itemprop="author" itemtype="https://schema.org/Person" itemscope><a class="url fn n" href="https://renaldisorders.com/archive/author/renaldisorders/" title="View all posts by renaldisorders" rel="author" itemprop="url"><span class="author-name" itemprop="name">renaldisorders</span></a></span></span> </div> </header> <div class="entry-content" itemprop="text"> <p><span style="font-weight: 400;">Diabetic nephropathy (DN) is the most common and serious complication of diabetes mellitus, with millions of people worldwide. CKD is the main cause of cfibrosis, hronic kidney disease, as well as end-stage renal disease, and confers extraordinary morbidity, mortality, and healthcare costs significantly different from those with normal kidney function. Although tremendous advances have been achieved in the management of hyperglycemia and hypertension, the two major risk factors for the development of DN, therapeutic approaches currently available are still insufficient to reverse the processes leading to progression of the disease in many patients. </span><span style="font-weight: 400;"><br /> </span><span style="font-weight: 400;"><br /> </span><span style="font-weight: 400;">Emerging interest is nowadays being directed toward finding new therapeutic targets driven by pathologic mechanisms involved in the disease, including inflammation, fibrosis, and oxidative stress. This review addresses the newest advances in therapeutic targets for diabetic nephropathy with a focus on pathways, molecules, and strategies presently studied that are believed to have the greatest impact on patient outcomes.</span></p> <h4><b>Role of inflammation in diabetic nephropathy</b></h4> <p><span style="font-weight: 400;">Inflammation is an important player in the progression of diabetic nephropathy and contributes to both glomerular as well as tubular injury. Increased levels of pro-inflammatory cytokines, chemokines, and adhesion molecules have been found in patients with DN, and it is directly related to the severity of renal impairment. Possibly, inflammation pathways may be exploited to prevent kidney damage.</span></p> <p><span style="font-weight: 400;">Several anti-inflammatory strategies have been explored:. For example, therapies targeting particular inflammatory molecules, such as interleukin-6 and transforming growth factor beta, have been shown to have potential in preclinical models. IL-6, a cytokine that acts as both a pro- and anti-inflammatory mediator, has been implicated in the regulation of ECM in the kidneys. Its activity inhibited had been demonstrated to decrease fibronectin and collagen IV production in mesangial cells, key markers of ECM accumulation that is considered a hallmark of DN progression.</span></p> <p><span style="font-weight: 400;">Except for its established and critical role as a profibrotic cytokine, TGF-β is known for promoting the production of ECM components that take part in renal fibrosis. Indeed, therapeutic strategies inhibiting TGF-β signaling have proven to be successful in reducing renal fibrosis, glomerular hypertrophy, and inflammation and slowing the progression of diabetic nephropathy. In this particular interest are inhibitors of the TGF-β/Smad3 pathway that are being considered for clinical use.</span></p> <p></div></div> <div style="background: #f7f7f7;border: 1px solid rgba(0, 0, 0, 0.07);"> <div style="padding: 30px;"><div class="Adblock-main"> <div class="Adblock-head"> <h2>Yearwise Publication Trend on <b>“<a href="https://renaldisorders.com/publication-trends/index/diabetic nephropathy" target="_blank" title="diabetic nephropathy - yearwise publication trends">diabetic nephropathy</a>”</b></h2> </div> </div><div class="results-container"><div class="chart-block" style="padding:15px;"> <div class="left"> <div id="results" class="results"></div> </div> <div class="right"> <div class="chart-container"><canvas id="publicationChart"></canvas></div> </div> <div class="keywordsdiv"> <div style="text-align:center;"><b>Find publication trends on relevant topics</b> </div> <span class="gp-icon icon-tags"><svg viewBox="0 0 512 512" aria-hidden="true" xmlns="http://www.w3.org/2000/svg" width="1em" height="1em"><path d="M20 39.5c-8.836 0-16 7.163-16 16v176c0 4.243 1.686 8.313 4.687 11.314l224 224c6.248 6.248 16.378 6.248 22.626 0l176-176c6.244-6.244 6.25-16.364.013-22.615l-223.5-224A15.999 15.999 0 00196.5 39.5H20zm56 96c0-13.255 10.745-24 24-24s24 10.745 24 24-10.745 24-24 24-24-10.745-24-24z"></path><path d="M259.515 43.015c4.686-4.687 12.284-4.687 16.97 0l228 228c4.686 4.686 4.686 12.284 0 16.97l-180 180c-4.686 4.687-12.284 4.687-16.97 0-4.686-4.686-4.686-12.284 0-16.97L479.029 279.5 259.515 59.985c-4.686-4.686-4.686-12.284 0-16.97z"></path></svg></span> <span id="keyword-stats"></span> </div> </div></div></div><div class="inside-article"><style> table { margin: 0 0 1.5em; 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Fibrosis leads to mass accumulation of ECM proteins, like collagen and fibronectin, within the kidneys’ glomeruli and interstitium. Effects are therefore multifaceted and include loss of kidney function, which is because both glomerulosclerosis and tubulointerstitial fibrosis will contribute to loss of kidney function.</span></p> <p><span style="font-weight: 400;">In recent years, the methods of targeted approaches aimed at inhibition of fibrosis have grown in importance in the research work of diabetic nephropathy. Among them is the blockade of the Wnt/β-catenin signaling pathway, which is also known to be directly related with the process of fibrogenesis. This pathway’s inhibition reportedly causes a decrease in the deposition of ECM in preclinical models. Other promised approaches lie in the blockers of matrix metalloproteinases, which would inhibit these enzymes for ECM remodeling, capable of slowing the velocity of fibrosis and preserving kidney function.</span></p> <p><span style="font-weight: 400;">An important research focus in fibrosis is along the line of mesangial cells that are responsible for producing and regulating the extracellular matrix within the glomerulus. Activated mesangial cells under high glucose levels produced higher levels of fibronectin as well as other extracellular matrix proteins. This process can be inhibited through modulation of key pathways, including the TGF-β/Smad3 axis or the PI3K/Akt pathway, to reduce the occurrence of fibrosis as well as improving renal outcomes in diabetic nephropathy.</span></p> <h4><b>SOCE: A Therapeutic Target for Calcium Storage</b></h4> <p><span style="font-weight: 400;">SOCE plays a crucial role in modulating the important functions of the renal tissue and mesangial cells. Current research has described SOCE as an ECE that contributes to the negative regulation of fibrosis and ECM production. Activation of SOCE was shown to repress the TGF-β/Smad3 pathway, which is heavily implicated in favoring the deposition of ECM. Inhibition of SOCE, on the other hand, led to increased expression of ECM proteins and heightened fibrosis.</span></p> <p><span style="font-weight: 400;">Disruption of SOCE could also be a potential approach to reducing the burden of fibrosis in diabetic nephropathy. Thapsigargin, the activator of SOCE, has been demonstrated to inhibit the synthesis of ECM components such as collagen IV and fibronectin in both in vitro and in vivo studies. Thus, altering SOCE might well be one of the potential therapeutic interventions to halt or potentially reverse kidney fibrosis in diabetic nephropathy.</span></p> <h4><b>Oxidative Stress Pathway in the Progression of DN</b></h4> <p><span style="font-weight: 400;">Oxidative stress is the primary element that mediates kidney damage from diabetic neuropathy. Hyperglycemia and the accompanying disturbances in metabolism evoke the excessive production of ROS, and the resulting cascade of actions instigates inappropriate reactions, like inflammation, apoptosis, and fibrosis. Replacing oxidative stress has, therefore, become a very important goal of therapeutic research on DN.</span></p> <p><span style="font-weight: 400;">Use of antioxidants may be a promising strategy, as antioxidants would scavenge ROS and thus protect renal cells from oxidative insults. A few antioxidants like NAC and PDTC have provided some therapeutic effects because of their ability to reduce oxidative stress and inhibit protein synthesis in the ECM. All these agents have the origin of ROS generation, like disturbed mitochondrial function and upregulation of the pro-oxidant enzyme NADPH oxidase.</span></p> <p><span style="font-weight: 400;">Promising results were obtained with drugs that modulate cellular pathways associated with oxidative stress, such as the nuclear factor erythroid 2-related factor 2 pathway. Activation of Nrf2 increases the expression of antioxidant enzymes and enhances the ability of the kidney to adapt to oxidative stress. Clinical trials of Nrf2 activators are under way in patients with diabetic nephropathy.</span></p> <p></div></div> <div style="background: #f7f7f7;border: 1px solid rgba(0, 0, 0, 0.07);"> <div style="padding: 30px;"><div class="Adblock-main"> <div class="Adblock-head"> <h2>Recent Publications on <b>“<a href="https://renaldisorders.com/recent-publications/index/diabetic nephropathy" target="_blank" rel="noopener" title="diabetic nephropathy - yearwise publication list">diabetic nephropathy</a>”</b></h2> </div> </div> <div class="pb-main"><div class="article-scroll"><div id="results_recent" class="results"></div></div><div class="keywordsdiv" style="margin: 0px 15px;margin-top:20px;"> <div style="text-align:center;"><b>Find publications on relevant topics</b> </div> <span class="gp-icon icon-tags"><svg viewBox="0 0 512 512" aria-hidden="true" xmlns="http://www.w3.org/2000/svg" width="1em" height="1em"><path d="M20 39.5c-8.836 0-16 7.163-16 16v176c0 4.243 1.686 8.313 4.687 11.314l224 224c6.248 6.248 16.378 6.248 22.626 0l176-176c6.244-6.244 6.25-16.364.013-22.615l-223.5-224A15.999 15.999 0 00196.5 39.5H20zm56 96c0-13.255 10.745-24 24-24s24 10.745 24 24-10.745 24-24 24-24-10.745-24-24z"></path><path d="M259.515 43.015c4.686-4.687 12.284-4.687 16.97 0l228 228c4.686 4.686 4.686 12.284 0 16.97l-180 180c-4.686 4.687-12.284 4.687-16.97 0-4.686-4.686-4.686-12.284 0-16.97L479.029 279.5 259.515 59.985c-4.686-4.686-4.686-12.284 0-16.97z"></path></svg></span> <span id="keyword-papers"></span> </div></div></div><div class="inside-article"> <style> .pb-main{ border: solid 1px #ccc; border-top: none; margin-bottom: 20px; padding-bottom: 25px; background:#fff; } .author-main { border: solid 1px #ccc; border-top: none; margin-bottom: 20px; padding-bottom: 25px; background:#fff; } .publication-block { padding: 10px; margin-bottom: 10px; background-color: #f9f9f9; text-align: left; background: #FFF; border-bottom: solid 1px #ccc; margin-left: 15px; margin-right: 15px; } 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"'"); str = str.replace(/\\'/g, "'"); str = str.replace(/\\'/g, "'"); return str; } function displayResults_recent(papers) { var resultsContainer = document.getElementById('results_recent'); if (!papers || papers.length === 0) { resultsContainer.innerHTML = '<p>No recent publications found.</p>'; return; } papers.forEach(paper => { var publicationBlock = document.createElement('div'); publicationBlock.className = 'publication-block'; var title_de = decodeString(paper.title); var publicationHTML = ` <div style="margin-bottom: 10px;line-height: 24px;"><a href="${paper.url}" target="_blank" title="${title_de}">${title_de}</a></div> <p><strong>Issue Release:</strong> ${paper.publishedDate}</p> `; publicationBlock.innerHTML = publicationHTML; resultsContainer.appendChild(publicationBlock); }); } function displayKeywordPapers(keywords) { var resultsContainer = document.getElementById('keyword-papers'); resultsContainer.innerHTML = ''; if (!keywords || keywords.length === 0) { resultsContainer.innerHTML = '<p>No data found.</p>'; return; } var keywordHTML = ''; keywords.forEach((key, index) => { let key_replace = key.replace(/ /g, '-'); key_replace = key_replace.toLowerCase(); keywordHTML += `<a href="https://renaldisorders.com/recent-publications/index/${key_replace}" target="_blank" title="${key} - publication list">${key}</a>`; if (index < keywords.length - 1) { keywordHTML += ', '; } }); resultsContainer.innerHTML = keywordHTML; } // Call the function with the PHP data var recent_papers = [ { "title": "Sodium Tungstate (NaW) Decreases Inflammation and Renal Fibrosis in Diabetic Nephropathy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38944202", "publishedDate": "2024" }, { "title": "Molecular mechanisms of diabetic nephropathy: A narrative review.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38946126", "publishedDate": "2024" }, { "title": "Preclinical antidiabetic and antioxidant effects of (benth.) harms in streptozotocin-induced diabetic nephropathy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38954410", "publishedDate": "2024" }, { "title": "Silk fibroin microspheres loaded Rehmannia Liuwei extract for the protection of endothelial cells from the inhibitory effects.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38878662", "publishedDate": "2024" }, { "title": "MiRNA-133a-3p Attenuates Renal Tubular Epithelial Cell Injury via Targeting MALM1 and Suppressing the Notch Signaling Pathway in Diabetic Nephropathy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38878099", "publishedDate": "2024" }, { "title": "EHHADH deficiency regulates pexophagy and accelerates tubulointerstitial injury in diabetic kidney disease.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38879653", "publishedDate": "2024" }, { "title": "Significant Association of Candidate Genes (AGTR1 and TGF-\u03921) Polymorphism with Diabetic Nephropathy in Diabetes Mellitus Type 2 Patients.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38852191", "publishedDate": "2024" }, { "title": "SB-525334 ameliorates renal injury in Diabetic Kidney Disease mouse model via suppressing inflammation.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38906377", "publishedDate": "2024" }, { "title": "Phenylsulfate-induced oxidative stress and mitochondrial dysfunction in podocytes are ameliorated by Astragaloside IV activation of the SIRT1\/PGC1\u03b1 \/Nrf1 signaling pathway.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38901196", "publishedDate": "2024" }, { "title": "Integrated network pharmacology and pharmacological investigations to discover the active compounds of Toona sinensis pericarps against diabetic nephropathy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38851471", "publishedDate": "2024" }, { "title": "Association of podocyte ultrastructural changes with proteinuria and pathological classification in type 2 diabetic nephropathy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38852840", "publishedDate": "2024" }, { "title": "miR-196a in the carcinogenesis and other disorders with an especial focus on its biomarker capacity.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38959626", "publishedDate": "2024" }, { "title": "Dysregulated Urinary Extracellular Vesicle Small RNAs in Diabetic Nephropathy: Implications for Diagnosis and Therapy.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38966710", "publishedDate": "2024" }, { "title": "Kidney tea [ (Blume) Miq.] improves diabetic nephropathy via regulating gut microbiota and ferroptosis.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38962302", "publishedDate": "2024" }, { "title": "Clinicopathological Characteristics and Disease Chronicity in Glomerular Diseases: A Decade-Long Study at Romania\\\\\\'s Largest Kidney Biopsy Reference Center.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38927350", "publishedDate": "2024" }, { "title": "CircRNA Arf3 suppresses glomerular mesangial cell proliferation and fibrosis in diabetic nephropathy via miR-107-3p\/Tmbim6 axis.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/39120858", "publishedDate": "2024" }, { "title": "CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/39116458", "publishedDate": "2024" }, { "title": "Prognostic significance of the hs-CRP\/Alb ratio for cardiovascular events in patients with end-stage renal disease undergoing maintenance hemodialysis.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/39114698", "publishedDate": "2024" }, { "title": "Mineralocorticoid receptor overactivation in diabetes mellitus: role of O-GlcNAc modification.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/38789539", "publishedDate": "2024" }, { "title": "Single-cell analysis provides new insights into the roles of tertiary lymphoid structures and immune cell infiltration in kidney injury and chronic kidney disease.", "url": "https:\/\/pubmed.ncbi.nlm.nih.gov\/39097168", "publishedDate": "2024" } ]; var keywordsArray = ["Diabetic nephropathy","therapeutic targets","inflammation","fibrosis","oxidative stress","renin-angiotensin system","store-operated calcium entry","TGF-\u03b2","SOCE","JAK\/STAT","biomarkers","glomerulosclerosis","novel therapies"]; displayResults_recent(recent_papers); displayKeywordPapers(keywordsArray); // function stripslashes(str) { // if (typeof str === 'string') { // return str.replace(/\/g, ''); // } // } </script></p> <h4><b>Angiotensin II and RAS Blockade Modulation</b></h4> <p><span style="font-weight: 400;">The renin-angiotensin system (RAS) is central to the regulation of blood pressure and fluid balance. In diabetic nephropathy, its overactivation plays a pivotal role. Angiotensin II is the main effector of RAS and enhances vasoconstriction, sodium retention, and inflammation, which are conducive to DN progression. RAS inhibition via ACE inhibitors and ARBs has been one of the cornerstones of DN therapy for several decades.</span></p> <p><span style="font-weight: 400;">Although RAS blockade is a cornerstone in clinical practice, many patients remain at risk for disease progression. This has opened new avenues to consider and investigate novel approaches beyond classic RAS inhibitors, including direct renin inhibition. Indeed, direct renin inhibition using aliskiren shows promise from preclinical studies through to early-phase clinical trials in reducing proteinuria and slowing the rate of progression of DN.</span></p> <p><span style="font-weight: 400;">Another potential strategy for treatment against DN is the concomitant blockade of RAS and the endothelin system. These two pathways are recognized factors in the perpetuation of vascular dysfunction and fibrosis in DN. Concomitant blockade of these pathways may prove to be more effective in controlling the factors driving kidney damage in diabetic nephropathy.</span></p> <h4><b>Targeting Novel Molecular Pathways</b></h4> <p><span style="font-weight: 400;">Other than the well-recognized therapeutic targets of DN, new molecular pathways are presently coming into identification. Those may later on present potential sites for intervention. One example of such pathways recently implicated in the pathogenesis of DN is the Notch signaling pathway. In excess is the overactivation of the podocytes toward this pathway, and such overactivation has been to contribute to fibrosis and sclerosis of the glomerulus. Notch signaling pathway inhibitors as potential candidates to develop protective effects against kidney injury are under research.</span></p> <p><span style="font-weight: 400;">The JAK/STAT pathway is another emerging therapeutic target in diabetic nephropathy. Its activation leads to inflammatory responses, fibrosis, and apoptosis of the kidney cells. Inhibitors of this pathway, such as baricitinib, have proven to reduce proteinuria and improve kidney function in preclinical models, and human trials have been initiated for their efficacy in patients.</span></p> <p><span style="font-weight: 400;">Apart from that, advancements in the study of biomarkers have enhanced the identification of patients at a high risk of developing DN and also guided the development of targeted therapies. Generally, markers like TNF receptors and kidney injury molecule-1 (KIM-1) are being researched to establish the role they play in predicting the advancement of disease and response to treatment that ensures more personalized approaches towards DN management.</span></p> <h4><b>Conclusion</b></h4> <p><span style="font-weight: 400;">Diabetic neuropathy remains a very challenging complication of diabetes, but numerous advances have been made in identifying and targeting the molecular mechanisms driving this disease. Attention to some particular pathways involving inflammation, fibrosis, oxidative stress, and others has led researchers to new therapies that may bring revolution in treatment strategies for DN. Thus, the potential future of DN treatment can be the combination of classical therapies such as RAS blockade and new targeted agents for single molecular pathways to be delivered to patients at risk for kidney failure.</span></p> <p></p> <h4><strong>References</strong></h4> <ol> <li>Zhang, Y., Jin, D., Kang, X., Zhou, R., Sun, Y., Lian, F. and Tong, X., 2021. <a href="https://www.frontiersin.org/articles/10.3389/fcell.2021.696542/full">Signaling pathways involved in diabetic renal fibrosis.</a> <i>Frontiers in cell and developmental biology</i>, <i>9</i>, p.696542.</li> <li>Rayego-Mateos, S., Morgado-Pascual, J.L., Opazo-Ríos, L., Guerrero-Hue, M., García-Caballero, C., Vázquez-Carballo, C., Mas, S., Sanz, A.B., Herencia, C., Mezzano, S. and Gómez-Guerrero, C., 2020. <a href="https://www.mdpi.com/1422-0067/21/11/3798">Pathogenic pathways and therapeutic approaches targeting inflammation in diabetic nephropathy.</a> <i>International journal of molecular sciences</i>, <i>21</i>(11), p.3798.</li> <li>Chaudhari, S., Yazdizadeh Shotorbani, P., Tao, Y., Davis, M.E., Mallet, R.T. and Ma, R., 2020. <a href="https://journals.physiology.org/doi/full/10.1152/ajprenal.00043.2020">Inhibition of interleukin-6 on matrix protein production by glomerular mesangial cells and the pathway involved.</a> <i>American Journal of Physiology-Renal Physiology</i>, <i>318</i>(6), pp.F1478-F1488.</li> <li>Donate-Correa, J., Luis-Rodríguez, D., Martín-Núñez, E., Tagua, V.G., Hernández-Carballo, C., Ferri, C., Rodríguez-Rodríguez, A.E., Mora-Fernández, C. and Navarro-González, J.F., 2020. <a href="https://www.mdpi.com/2077-0383/9/2/458">Inflammatory targets in diabetic nephropathy. </a><i>Journal of Clinical Medicine</i>, <i>9</i>(2), p.458.</li> <li>Chaudhari, S., Li, W., Wang, Y., Jiang, H., Ma, Y., Davis, M.E., Zuckerman, J.E. and Ma, R., 2017. <a href="https://journals.physiology.org/doi/full/10.1152/ajprenal.00483.2016">Store-operated calcium entry suppressed the TGF-β1/Smad3 signaling pathway in glomerular mesangial cells.</a> <i>American Journal of Physiology-Renal Physiology</i>, <i>313</i>(3), pp.F729-F739.</li> <li>Shotorbani, P.Y., Chaudhari, S., Tao, Y., Tsiokas, L. and Ma, R., 2020. <a href="https://journals.physiology.org/doi/full/10.1152/ajprenal.00508.2019">Inhibitor of myogenic differentiation family isoform a, a new positive regulator of fibronectin production by glomerular mesangial cells.</a> <i>American Journal of Physiology-Renal Physiology</i>, <i>318</i>(3), pp.F673-F682.</li> </ol> <p></div></div> <div style="background: #f7f7f7;border: 1px solid rgba(0, 0, 0, 0.07);"> <div style="padding: 30px;"><div class="Adblock-main"> <div class="Adblock-head"> <h2>Top Experts on “<b style="color:#000;font-size:22px;">diabetic nephropathy</b>“</h2> </div> </div><div class="author-main"><div id="results_author"></div><div style="text-align: center;"><a class="register-button" href="https://renaldisorders.com/expert-search" target="_blank" rel="noopener">Find experts on any field</a></div></div><div class="inside-article" style="background: none;border: none;box-shadow: none;margin-top: -70px;"> <style> .author-block { padding: 15px; 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", "email": "tokeshi@eng.hokudai.ac.jp", "slug_tail": "m-tokeshi" } }; //console.log(authors_data); displayResults_author(authors_data); var keywordsArray = ["Diabetic nephropathy","therapeutic targets","inflammation","fibrosis","oxidative stress","renin-angiotensin system","store-operated calcium entry","TGF-\u03b2","SOCE","JAK\/STAT","biomarkers","glomerulosclerosis","novel therapies"]; displayKeywordAuthors(keywordsArray); </script></p> </div> <footer class="entry-meta" aria-label="Entry meta"> <span class="cat-links"><span class="gp-icon icon-categories"><svg viewBox="0 0 512 512" aria-hidden="true" xmlns="http://www.w3.org/2000/svg" width="1em" height="1em"><path d="M0 112c0-26.51 21.49-48 48-48h110.014a48 48 0 0143.592 27.907l12.349 26.791A16 16 0 00228.486 128H464c26.51 0 48 21.49 48 48v224c0 26.51-21.49 48-48 48H48c-26.51 0-48-21.49-48-48V112z" /></svg></span><span class="screen-reader-text">Categories </span><a 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