Is bariatric surgery improving mitochondrial function in the renal cells of patients with obesity-induced kidney disease?. (November 2022)

• Record Type: Journal Article
• Authors: Cañizares, Stalin; Guaillas, Auki; Velarde, Francesca; de Vaca, Verónica Cabeza; Terán, Fuad; Caicedo, Andrés
• Is Part Of: Pharmacological research. Volume 185(2022)
• Publication Date: 2022-11
• Subjects: BS bariatric surgery -- T2D type 2 diabetes -- HTN arterial hypertension -- ROS reactive oxygen species -- ATP adenosine triphosphate -- RYGB roux-en-y-gastric-bypass -- SG sleeve gastrectomy -- TNF-ɑ tumor necrosis factor alpha -- IL-1β interleukin-1β -- IL-6 interleukin-6 -- CKD chronic kidney disease -- AGEs advanced glycation end products -- SGLT2 sodium-glucose co-transporter 2 -- GFR glomerular filtration rate -- eGFR estimated glomerular filtration rate -- BUN blood urea nitrogen -- NGAL neutrophil gelatinase-associated lipocalin -- COX-IV cytochrome c oxidase subgroup IV -- AMPK adenosine monophosphate-activated protein kinase -- MFN1–2 mitofusin protein 1 and 2 -- OPA1 opacity associated protein 1 -- DRP1 dynamin related protein 1 -- FIS1 mitochondrial fission 1 protein -- NLRP3 NLR family pyrin domain containing 3 protein -- PINK1 PTEn induced kinase 1 -- PRKN parkin RBR E3 ubiquitin protein ligase -- TGF-β1 transforming growth factor beta 1 -- PGC-1ɑ peroxisome proliferator-activated receptor ɑ coactivator-1 -- NRF1 nuclear respiratory factor 1 -- NRK2 nicotinamide ribose kinase 2 -- NAD+ nicotinamide adenine dinucleotide (oxidized form) -- IRI ischemia-reperfusion injury -- NAM NAD precursor niacinamide -- HCAR2 hydroxycarboxylic acid receptor 2 -- AKI acute kidney injury -- NAMPT nicotinamide phosphoribosyltransferase -- PGE2 prostaglandin E2 -- TFAM or mtTFA mitochondrial transcription factor A -- mTORC1 mammalian target of rapamycin complex 1 -- SIRT1–7 sirtuin protein 1–7 -- JNK c-JUN N-terminal kinase -- SMAD3 smad family member 3 -- miRNA micro ribonucleic acids -- lncRNAs long noncoding ribonucleic acids -- Tug taurine upregulated 1 -- GLP-1 glucagon-like peptide 1 -- RAS renin-angiotensin system -- UACR urine albumin-to-creatinine ratio -- BPD biliopancreatic diversion -- LFD low fat diet -- HFD high fat diet -- MDCT multidetector computed tomographies -- BOLD-MRI blood oxygen level dependent magnetic resonance imaging -- ACR albuminuria-to-creatininuria ratio -- ND1 nicotinamide adenine dinucleotide dehydrogenase subunit-1 -- PCR polymerase chain reaction -- TLR-9 toll-like receptor 9 -- ANP atrial natriuretic peptide -- ETC electron transport chain -- NADH nicotinamide adenine dinucleotide (NAD) + hydrogen (H) -- PYY peptide YY -- CCK cholecystokinin -- GIP gastric inhibitory peptide -- HIF-1 hypoxia inducible factor 1 -- PDX-1 pancreatic and duodenal homeobox 1; Bariatric surgery -- Mitochondria -- Mitochondrial function -- Renal cells -- Obesity-induced kidney disease -- Chronic kidney disease; Pharmacology -- Periodicals; Pharmacology -- Periodicals; Research -- Periodicals; Médicaments -- Recherche -- Périodiques; Pharmacologie -- Périodiques; 615.105
• DOI: 10.1016/j.phrs.2022.106488
• Languages: English
• ISSNs: 1043-6618

Abstract

Abstract: The role of mitochondria in health and disease has dramatically changed in the last decade. Its complex integration into cell physiology is comprised of key metabolic functions of great importance in health maintenance. Treating obesity seems to improve overall mitochondria tissue malfunction; however, the extent of their impact on patients remains elusive due to the lack of follow-up studies. It has been observed that procedures such as bariatric surgery (BS) can modify how our body absorbs nutrients, influencing metabolic processes and mitochondrial function in several cells and tissues. In fact, tissue analysis performed in vivo and in patients support that BS mitigates mitochondrial dysfunction in obese subjects. BS has been observed to reduce the presence of comorbidities such as type 2 diabetes (T2D) and hypertension (HTN) in patients. It is still unclear how BS specifically affects mitochondrial dynamics in obesity-induced comorbidities such as kidney disease. This article provides insightful information regarding the amelioration of mitochondrial dynamics in renal cells and systems after BS. Understanding the multiple pathways that lead to mitochondrial dysregulation in obesity-related kidney disease and relating them to the positive molecular changes after BS may lead to the development of adjuvant therapies to control this and other conditions with similar pathophysiological backgrounds. Graphical Abstract: ga1 Highlights: Treating obesity improves mitochondria dysfunction; however, many aspects of metabolic recovery still remain elusive. Bariatric surgery (BS) can modify our metabolic processes including mitochondrial function in diverse cells and tissues. BS seems to positively affect mitochondrial dynamics in obesity-induced kidney disease (OIKD). From basic science to clinical aspects, we analyze the amelioration of mitochondrial dynamics in OIKD. Understanding the mitochondrial changes in renal disease may lead to the development of better therapies.