The Molecular Mechanism of Renal Tubulointerstitial Inflammation Promoting Diabetic Nephropathy

Abstract

Rui Xue,1,* Haiting Xiao,2,* Vinod Kumar,3 Xiqian Lan,2 Ashwani Malhotra,4 Pravin C Singhal,4 Jianning Chen1 1Affiliated Mental Health Center & Hangzhou Seventh People’s Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310000, People’s Republic of China; 2Key Laboratory of Luzhou City for Aging Medicine, Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, Sichuan, 646000, People’s Republic of China; 3Department of Dermatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India; 4Feinstein Institute for Medical Research and Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, NY, 11030, USA*These authors contributed equally to this workCorrespondence: Jianning Chen; Pravin C Singhal, Email [email protected]; [email protected]: Diabetic nephropathy (DN) is a common complication affecting many diabetic patients, leading to end-stage renal disease. However, its pathogenesis still needs to be fully understood to enhance the effectiveness of treatment methods. Traditional theories are predominantly centered on glomerular injuries and need more explicit explanations of recent clinical observations suggesting that renal tubules equally contribute to renal function and that tubular lesions are early features of DN, even occurring before glomerular lesions. Although the conventional view is that DN is not an inflammatory disease, recent studies indicate that systemic and local inflammation, including tubulointerstitial inflammation, contributes to the development of DN. In patients with DN, intrinsic tubulointerstitial cells produce many proinflammatory factors, leading to medullary inflammatory cell infiltration and activation of inflammatory cells in the interstitial region. Therefore, understanding the molecular mechanism of renal tubulointerstitial inflammation contributing to DN injury is of great significance and will help further identify key factors regulating renal tubulointerstitial inflammation in the high glucose environment. This will aid in developing new targets for DN diagnosis and treatment and expanding new DN treatment methods.Keywords: diabetic nephropathy, renal tubules, renal tubular injury, renal tubulointerstitial inflammation, DN injury

Keywords

• diabetic nephropathy
• renal tubules
• renal tubular injury
• renal tubulointerstitial inflammation
• dn injury