Cell Membrane Labeled as an “Additional Reason” For Aging, Fascinating New Research-2024
Professor Keiko Kono, head of the Membranology unit and senior author of this work, recalls that his sole purpose for this investigation was to study the healing mechanism of cell membranes.
Just like plants we humans also have a cellular structure that needs to protect the DNA and organelles inside, but our cells do not possess a cell wall instead it has a membrane.
Our cells are protected by a thin membrane that is only 5 nanometers thick, or 1/20th the thickness of a soap bubble.
Cell Membrane Labeled Functions are;
Normal physiological processes, such as muscle contractions and tissue traumas, might harm this barrier. So we always need an aware state of mind because even the smallest injuries can cause deeper problems but miraculously to compensate for this weakness, cells have remolding mechanisms that can partially heal damaged cell membranes.
It was often thought that mechanical injury to the cell membrane resulted in one of two obvious biological outcomes:
- Recuperation or death.
- Cellular senescence,
But the third result was surprising
Research By Professor Keiko Kono Regarding “Cell Membrane’s Responsible For Aging”
Professor Keiko Kono, head of the Membranology unit and senior author of this work, recalls that his sole purpose for this investigation was to study the healing mechanism of cell membranes.
Several members of the team, including Kojiro Suda, Yohsuke Moriyama, Nurhanani Razali, and colleagues, were involved in the research.
Surprisingly, they found that disruption to the cell membrane can change the fate of the cell.
The degree and the type of damage and the influx of calcium ions are crucial in deciding the destiny of the cells.
The damage to the narrow cell membrane can be readily repaired, enabling the cells to divide without any issues.
Cell death is induced by the highest degree of damage to the cell membrane.
Even if membrane resealing appears to be successful, a moderate degree of damage to the cell membrane causes the cells to become dying cells a few hours later.
Cancer cells proliferate indefinitely.
Normal, non-cancerous cells, on the other hand, have a limited ability to divide; they can only do so up to 50 times till division is irrevocably halted and they enter a condition called cellular senescence.
Even though they still have a metabolism, senescent cells secrete different proteins that trigger immunological responses in neighboring tissues and organs that are distant.
This is in contrast to youthful, healthy cells. This process can cause both positive and negative changes in our bodies, such as aging, the promotion of cancer, and the acceleration of wound healing.
Numerous investigations conducted over the past years have revealed the existence of declining cells in animal bodies, including human bodies, and the ability to restore bodily functioning in experimental animals by removing these cells.
Still up for debate, though, is what causes cell senescence in the human body.
Professor Kono says that the origin of senescent cells in our bodies comes particularly from those near the injured tissues, and can be explained by cell membrane destruction, based on the gene expression profile and bioinformatics analysis.
Repeated cell division is the most well-established inducer of cellular senescence.
In a lab setting, a variety of other stressors, including damaged DNA, carcinogen activation, and epigenetic shifts, also cause cellular senescence.
The science kingdom has always accepted the wisdom that different stimuli can eventually cause cellular senescence by triggering the DNA damage response,
so they discovered that after cell membrane damage calcium influx can increase along with the p53 gene which can cause senescence in the cell.
Gene p53 is a tumor suppressor gene that is crucial for the health of cellular activity and other bodily functions. The presence of the gene can stop the tumors from growing and hence can control/prevent abnormal cell growth.
Evidence-Based Research Paper: https://www.nature.com/articles/s43587-024-00575-6
