Autophagy for cells, kidneys and personal health and longevity

Renal protection and renal recovery depends on the  Trinity following:

1.  Reduced oxidative stress or increased antioxidant enzyme capacity. (Nrf2 2 activators.)

2.  Reduced neuroimmune stress, (vagal activation of cholinergic anti inflammatory pathway, repair of leaky gut with homemade yogurt.)

3.  Autophagy.

Autophagy promoters include the following:

1.  Fat burning producing beta hydroxybutyrate ( ketodiet, fasting, lactate producing exercise.)

2.  Spermidine (2 tablespoons of wheat germ daily.)

3.  Sulforaphane (Broccoli sprouts or other Nrf2 activation, H2, melatonin, Mediterranean diet.)

I was impressed by Wu and Wang in this review on autophagy and chronic kidney disease.  The renal protective and recovery factors listed  for acute and chronic kidney disease is congruent with renal recovery which depends on,at least, the Trinity of factors above. All  three factors should be synergistic and protective.  

Every aging kidney would benefit.  So would every aging cell.

https://www.mdpi.com/2073-4409/8/1/61/htm

Autophagy in Chronic Kidney Diseases

Tien-An Lin

Cells 2019, 8(1), 61; doi:

Review

Victor Chien-Chia Wu ² and Chao-Yung Wang ^2,3,*

¹

Department of General Surgery, Chang Gung Memorial Hospital, Taoyuan City 333, Taiwan

²

Department of Cardiology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taoyuan City 333, Taiwan

³

Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan 350, Taiwan

^*

Author to whom correspondence should be addressed. 

Received: 8 December 2018 / Accepted: 9 January 2019 / Published: 16 January 2019

Abstract

:

Autophagy is a cellular recycling process involving self-degradation and reconstruction of damaged organelles and proteins. Current evidence suggests that autophagy is critical in kidney physiology and homeostasis. In clinical studies, autophagy activations and inhibitions are linked to acute kidney injuries, chronic kidney diseases, diabetic nephropathies, and polycystic kidney diseases. Oxidative stress, inflammation, and mitochondrial dysfunction, which are implicated as important mechanisms underlying many kidney diseases, modulate the autophagy activation and inhibition and lead to cellular recycling dysfunction. Abnormal autophagy function can induce loss of podocytes, damage proximal tubular cells, and glomerulosclerosis. After acute kidney injuries, activated autophagy protects tubular cells from apoptosis and enhances cellular regeneration. Patients with chronic kidney diseases have impaired autophagy that cannot be reversed by hemodialysis. Multiple nephrotoxic medications also alter the autophagy signaling, by which the mechanistic insights of the drugs are revealed, thus providing the unique opportunity to manage the nephrotoxicity of these drugs. In this review, we summarize the current concepts of autophagy and its molecular aspects in different kidney cells pathophysiology. We also discuss the current evidence of autophagy in acute kidney injury, chronic kidney disease, toxic effects of drugs, and aging kidneys. In addition, we examine therapeutic possibilities targeting the autophagy system in kidney diseases.